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Role of peroxisome proliferator-activated receptor alpha in neurodegenerative diseases and other neurological disorders:Clinical application prospects 认领 引用
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作者 Zijun Wu Yuying Zhao +3 位作者 Shujing Hao Mengyao An Chengcheng Song Jing Li 《Neural Regeneration Research》 SCIE CAS CSCD 2026年第4期1468-1482,共15页
Peroxisome proliferator-activated receptor alpha is a member of the nuclear hormone receptor superfamily and functions as a transcription factor involved in regulating cellular metabolism.Previous studies have shown t... Peroxisome proliferator-activated receptor alpha is a member of the nuclear hormone receptor superfamily and functions as a transcription factor involved in regulating cellular metabolism.Previous studies have shown that PPARαplays a key role in the onset and progression of neurodegenerative diseases.Consequently,peroxisome proliferator-activated receptor alpha agonists have garnered increasing attention as potential treatments for neurological disorders.This review aims to clarify the research progress regarding peroxisome proliferator-activated receptor alpha in nervous system diseases.Peroxisome proliferator-activated receptor alpha is present in all cell types within adult mouse and adult neural tissues.Although it is conventionally believed to be primarily localized in the nucleus,its function may be regulated by a dynamic balance between cytoplasmic and nuclear shuttling.Both endogenous and exogenous peroxisome proliferator-activated receptor alpha agonists bind to the peroxisome proliferator-activated response element to exert their biological effects.Peroxisome proliferator-activated receptor alpha plays a significant therapeutic role in neurodegenerative diseases.For instance,peroxisome proliferator-activated receptor alpha agonist gemfibrozil has been shown to reduce levels of soluble and insoluble amyloid-beta in the hippocampus of Alzheimer's disease mouse models through the autophagy-lysosomal pathway.Additionally,peroxisome proliferator-activated receptor alpha is essential for the normal development and functional maintenance of the substantia nigra,and it can mitigate motor dysfunction in Parkinson's disease mouse models.Furthermore,peroxisome proliferator-activated receptor alpha has been found to reduce neuroinflammation and oxidative stress in various neurological diseases.In summary,peroxisome proliferator-activated receptor alpha plays a crucial role in the onset and progression of multiple nervous system diseases,and peroxisome proliferator-activated receptor alpha agonists hold promise as new therapeutic agents for the treatment of neurodegenerative diseases,providing new options for patient care. 展开更多
关键词 agonists Alzheimer's disease gut microbiota multiple sclerosis nervous system disease neurodegeneration neurodegenerative disease neuroinflammation Parkinson's disease peroxisome proliferator-activated receptor alpha
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Lianhe Xiaozhi ointment ameliorates metabolic dysfunctionassociated steatotic liver disease via peroxisome proliferatoractivated receptor alpha pathway activation 认领 引用
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作者 Li-Juan Nie Gao-Xiang Wang +6 位作者 Xin-Yi Yang Jing Sun Yu-Tian Cao Yan Lou Yi-Fan Lu Jiang-Yi Yu Xi-Qiao Zhou 《World Journal of Gastroenterology》 SCIE CAS 2026年第9期124-143,共20页
BACKGROUND Lianhe Xiaozhi ointment(LXO),an innovative formulation derived from the classic Huanglian Wendan decoction,has been granted a national invention patent.With increasing years of clinical expertise within the... BACKGROUND Lianhe Xiaozhi ointment(LXO),an innovative formulation derived from the classic Huanglian Wendan decoction,has been granted a national invention patent.With increasing years of clinical expertise within the Jiangsu Province Hospital of Chinese Medicine in China,LXO has become increasingly recognized as a potent remedy for metabolic disorders,particularly metabolic dysfunction-associated steatotic liver disease(MASLD).To date,specific bioactive components and underlying mechanisms remain unclear.AIM To determine the bioactive components of LXO and clarify its mechanisms of action relevant to management of MASLD.METHODS We used ultra-high performance liquid chromatography with quadrupole time-of-flight mass spectrometry and network pharmacology approaches to systematically determine the key bioactive components of LXO and elucidate biological pathways modulated in the treatment of MASLD.Critical signaling pathways were also elucidated via hepatic transcriptomic analysis,and an exhaustive and rigorous exploration of the therapeutic efficacy and underlying mechanisms of LXO in MASLD was conducted via a combination of in vivo and in vitro high-fat model experiments.RESULTS Network pharmacology analysis revealed six pivotal bioactive components within LXO that collectively serve as the cornerstone for their efficacy against MASLD.LXO exerts multiple therapeutic effects,including weight gain retardation,amelioration of glucose and lipid metabolism disturbances,liver injury mitigation,hepatic inflammation alleviation,and correction of gut microbiota disorders.Multiple platform analyses,including hepatic transcriptomics,quantitative real-time polymerase chain reaction,and western blotting,confirmed that LXO induces peroxisome proliferator-activated receptor alpha(PPARα)transcriptional activation in the liver.In vitro studies confirmed that a PPARαantagonist markedly diminishes the lipid-lowering capacity of LXO.CONCLUSION Collectively,our findings suggest that LXO exerts therapeutic effects on high-fat diet-induced MASLD at least in part via PPARαpathway activation. 展开更多
关键词 Metabolic dysfunction-associated steatotic liver disease Traditional Chinese medicine Peroxisome proliferator-activated receptor alpha Inflammation Network pharmacology
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Peroxisome-mitochondria contact-mediated ROS transfer:A key line of defence under plant stress 认领 引用
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作者 Jia Song Zhijie Gao Hongliang Xu 《Advanced Agrochem》 CAS CSCD 2026年第1期4-6,共3页
Reactive oxygen species(ROS)act as early messengers in plants exposed to drought,salinity,heat and other environmental challenges.Their timely removal is crucial.Unchecked ROS injure membranes,macromolecules and photo... Reactive oxygen species(ROS)act as early messengers in plants exposed to drought,salinity,heat and other environmental challenges.Their timely removal is crucial.Unchecked ROS injure membranes,macromolecules and photosynthetic systems,ultimately curbing growth or causing cell death.While mitochondria possess inhouse antioxidant machinery,how non-mitochondrial systems contribute to mitochondrial redox homeostasis has remained unresolved.Laura F.DiGiovanni et al.demonstrate that peroxisomes directly protect mitochondria through contact-mediated ROS shuttling.This discovery extends the concept of organelle crosstalk beyond metabolic exchange to contact-mediated ROS flux,adding a system-level buffer against oxidative stress.Deep understanding and regulation of this pathway are highly significant for exploring how ROS coordinate plant stress responses,enhancing crop stress resistance and reducing extreme environment-induced oxidative damage.This may provide breeders and agronomists with a novel approach to develop stress-resistant traits. 展开更多
关键词 Mitochondria Peroxisome Reactive oxygen species Redox homeostasis Plant stress tolerance
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Conjugated linoleic acid isomers and their precursor fatty acids regulate peroxisome proliferator-activated receptor subtypes and major peroxisome proliferator responsive element-bearing target genes in HepG2 cell model 认领 引用 被引量：1
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作者 Sailas BENJAMIN Silke FLOTHO +1 位作者 Torsten BRCHERS Friedrich SPENER 《Journal of Zhejiang University-SCIENCE B》 SCIE CAS CSCD 2013年第2期115-123,共9页
The purpose of this study was to examine the induction profiles （as judged by quantitative reverse tran- scription polymerase chain reaction （qRT-PCR）） of peroxisome proliferator-activated receptor （PPAR） α,β,... The purpose of this study was to examine the induction profiles （as judged by quantitative reverse tran- scription polymerase chain reaction （qRT-PCR）） of peroxisome proliferator-activated receptor （PPAR） α,β, y subtypes and major PPAR-target genes bearing a functional peroxisome proliferator responsive element （PPRE） in HepG2 cell model upon feeding with cis-9,trans-11-octadecadienoic acid （9-CLA） or trans-10,cis-12-octadecadienoic acid （10-CLA） or their precursor fatty acids （FAs）. HepG2 cells were treated with 100 pmol/L 9-CLA or 10-CLA or their precursor FAs, viz., oleic, linoleic, and trans-11-vaccenic acids against bezafibrate control to evaluate the induc- tion/expression profiles of PPAR （α, β, γ subtypes and major PPAR-target genes bearing a functional PPRE, i.e., fatty acid transporter （FAT）, glucose transporter-2 （GLUT-2）, liver-type FA binding protein （L-FABP）, acyl CoA oxidase-1 （ACOX-1）, and peroxisomal bifunctional enzyme （PBE） with reference to β-actin as house keeping gene. Of the three housekeeping genes （glyceraldehyde 3-phosphate dehydrogenase （GAPDH）, β-actin, and ubiquitin）, β-actin was found to be stable. Dimethyl sulfoxide （DMSO）, the common solubilizer of agonists, showed a significantly higher induction of genes analyzed, qRT-PCR profiles of CLAs and their precursor FAs clearly showed upregulation of FAT, GLUT-2, and L-FABP （-0.5-.0-fold）. Compared to 10-CLA, 9-CLA decreased the induction of the FA metabolizing gene ACOX-1 less than did PBE, while 10-CLA decreased the induction of PBE less than did ACOX-I. Both CLAs and precursor FAs upregulated PPRE-beadng genes, but with comparatively less or marginal activation of PPAR subtypes This indicates that the binding of CLAs and their precursor FAs to PPAR subtypes results in PPAR activation, thereby induction of the target transporter genes coupled with downstream lipid metabolising genes such as ACOX-1 and PBE. To sum up, the expression profiles of these candidate genes showed that CLAs and their precursor FAs are involved in lipid signalling by modulating the PPAR a, 13, or ~ subtype for the indirect activation of the PPAR-target genes, which may in turn be responsible for the supposed health effects of CLA, and that care should be taken while calculating the actual fold induction values of candidate genes with reference to housekeeping gene and DMSO as they may impart false positive results. 展开更多
关键词 Conjugated linoleic acid HepG2 cell model qRT-PCR Peroxisome proliferator-activated receptor Peroxisome proliferator responsive element-bearing genes Lipid agonists
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Effect of insulin and metformin on methylation and glycolipid metabolism of peroxisome proliferator-activated receptor γcoactivator-1A of rat offspring with gestational diabetes mellitus 认领 引用 被引量：13
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作者 Ai-Qin Song Li-Rong Sun +2 位作者 Yan-Xia Zhao Yan-Hua Gao Lei Chen 《Asian Pacific Journal of Tropical Medicine》 SCIE CAS 2016年第1期89-93,共5页
Objective:To discuss the effect of insulin and metformin on amethylation and glycolipid metabolism of peroxisome proliferator-activated receptor γ coactivator-1A(PPARGC1A) of rat offspring with gestational diabetes m... Objective:To discuss the effect of insulin and metformin on amethylation and glycolipid metabolism of peroxisome proliferator-activated receptor γ coactivator-1A(PPARGC1A) of rat offspring with gestational diabetes mellitus(GDM).Methods:A total of 45 pregnant rats received the intraperitoneal injection of streptozotocin to establish the pregnant rat model of GDM.A total of 21 pregnant rats with GDM were randomly divided into three groups,with 7ruts in each group,namely the insulin group,metformin group and control group.Rats in the insulin group received the abdominal subcutaneous injection of 1 mL/kg recombinant insulin glargine at 18:00 every day.Rats in the metformin group received the intragastric infusion of metformin hydrochloride at 18:00 every day,with the first dose of 300 mg/kg.The doses of two groups were adjusted every 3 d to maintain the blood glucose level at 2.65-7.62 mmol/L.Rats in the control group received the intragastric infusion of 1 mL normal saline at 18:00 every day.After the natural delivery of pregnant rats.10 offspring rats were randomly selected from each group.At birth,4 wk and 8 wk after the birth of offspring rats,the weight of offspring rats was measured.The blood glucose level of offspring rats was measured at 4wk and 8 wk,while the level of serum insulin,triglyceride and leptin was measured at 8 wk.Results:The weight of offspring rats at birth in the insulin group and metformin group was significantly lower than the one in the control group(P0.05).The fasting blood glucose and random blood glucose in the insulin group and metformin group at 4 wk and 8 wk were all significantly lower than ones in the control group(P0.05).The expression of PPARGC1 A mRNA in the insulin group and metformin group was significantly higher and the methylation level of PPARGC1 A was significantly lower than the one in the control group(P0.05).Insulin and leptin at 8 wk in the insulin group and metformin group were significantly higher,while triglyceride was significantly lower than the one in the control group(P0.05).Conclusions:GDM can induce the methylation of PPARGC1 A of offspring rats to reduce the expression of PPARGC1 A mRNA and then cause the disorder of glycolipid metabolism when the offspring rats grow up;the insulin or metformin in the treatment of pregnant rats with GDM can reduce the methylation level of PPARGC1 A and thus improve the abnormal glycolipid metabolism of offspring rats. 展开更多
关键词 Insulin Metformin Gestational diabetes mellitus Peroxisome proliferator-activated receptor γ coactivator-1 A Methylation Glycolipid metabolism
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Pro12Ala polymorphism of the peroxisome proliferator-activated receptor γ2 in patients with fatty liver diseases 认领 引用 被引量：12
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作者 Johannes W Rey Andrea Noetel +6 位作者 Aline Hardt Ali Canbay Hakan Alakus Axel zur Hausen Hans Peter Dienes Uta Drebber Margarete Odenthal 《World Journal of Gastroenterology》 SCIE CAS 2010年第46期5830-5837,共8页
AIM:To test the occurrence of the Pro12Ala mutation of the peroxisome proliferator-activated receptor-γ (PPARγ)2-gene in patients with non-alcoholic fatty liver disease (NAFLD) or alcoholic fatty liver disease (AFLD... AIM:To test the occurrence of the Pro12Ala mutation of the peroxisome proliferator-activated receptor-γ (PPARγ)2-gene in patients with non-alcoholic fatty liver disease (NAFLD) or alcoholic fatty liver disease (AFLD).METHODS:DNA from a total of 622 specimens including 259 blood samples of healthy blood donors and 363 histologically categorized liver biopsies of patients with NAFLD (n=263) and AFLD (n=100) were analyzed by Real-time polymerase chain reaction using allele-specific probes.RESULTS:In the NAFLD and the AFLD collective,3% of the patients showed homozygous occurrence of the Ala12 PPARγ2-allele,differing from only 1.5% cases in the healthy population.In NAFLD patients,a high incidence of the Ala12 mutant was not associated with the progression of fatty liver disease.However,we observed a significantly higher risk (odds ratio=2.50,CI:1.05-5.90,P=0.028) in AFLD patients carrying the mutated Ala12 allele to develop inflammatory alterations.The linkage of the malfunctioning Ala12-positive PPARγ2 isoform to an increased risk in patients with AFLD to develop severe steatohepatitis and fibrosis indicates a more prominent anti-inflammatory impact of PPARγ2 in progression of AFLD than of NAFLD.CONCLUSION:In AFLD patients,the Pro12Ala single nuclear polymorphism should be studied more extensively in order to serve as a novel candidate in biomarker screening for improved prognosis. 展开更多
关键词 Single nucleotide polymorphism Peroxisome proliferator-activated receptor γ Non-alcoholic steatohepatitis Alcoholic steatohepatitis Inflammation Fibrosis Hepatitis Steatosis Steatohepatitis
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Peroxisome proliferator-activated receptor gamma inhibits hepatic fibrosis in rats 认领 引用 被引量：22
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作者 Zheng Wang Jia-Peng Xu +4 位作者 Yong-Chao Zheng Wei Chen Yong-Wei Sun Zhi-YongWu Meng Luo 《Hepatobiliary & Pancreatic Diseases International》 SCIE CAS 2011年第1期64-71,共8页
BACKGROUND:Hepatic fibrosis is a necessary step in the development of hepatic cirrhosis.In this study we used lentiviral vector-mediated transfection technology to evaluate the effect of peroxisome proliferator-activa... BACKGROUND:Hepatic fibrosis is a necessary step in the development of hepatic cirrhosis.In this study we used lentiviral vector-mediated transfection technology to evaluate the effect of peroxisome proliferator-activated receptor gamma(PPAR-γ)on rat hepatic fibrosis.METHODS:Hepatic fibrosis in rats was induced by CCl4 for 2 weeks(early fibrosis)and 8 weeks(sustained fibrosis).The rats were randomly divided into four groups:normal control,fibrosis,blank vector,and PPAR-γ.They were infected with the recombinant lentiviral expression vector carrying the rat PPAR-γgene by portal vein injection.The liver of the rats was examined histologically and hydroxyproline was assessed.In vitro primary hepatic stellate cells(HSCs)were infected with the recombinant lentiviral expression vector carrying the rat PPAR-γgene.The status of HSC proliferation was measured by the MTT assay.The protein levels of PPAR-γ,α-smooth muscle actin(α-SMA)and type I collagen expression were evaluated by the Western blotting method.RESULTS:In vitro studies revealed that expression of PPAR-γinhibited expression ofα-SMA and type I collagen in activated HSCs(P<0.01)as well as HSC proliferation(P<0.01).In vivo experiments indicated that in the early hepatic fibrosis group,the hydroxyproline content and the level of collagen I protein in the liver in the PPAR-γtransfected group were not significantly different compared to the hepatic fibrosis group and the blank vector group;whereas the expressions of PPAR-γandα-SMA were different compared to the hepatic fibrosis group(P<0.01).In the sustained hepatic fibrosis group,there were significant differences in the hydroxyproline content and the expression of PPAR-γ,α-SMA,and type I collagen between each group.CONCLUSION:PPAR-γcan inhibit HSC proliferation and hepatic fibrosis,and suppressα-SMA and type I collagen expression. 展开更多
关键词 peroxisome proliferator-activated receptor gamma hepatic fibrosis hepatic stellate cells lentiviral vector
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Role of peroxisome proliferators-activated receptors in the pathogenesis and treatment of nonalcoholic fatty liver disease 认领 引用 被引量：35
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作者 Eric R Kallwitz Alan McLachlan Scott J Cotler 《World Journal of Gastroenterology》 SCIE CAS 2008年第1期22-28,共7页
Nonalcoholic fatty liver disease （NAFLD） is highly prevalent and can result in nonalcoholic steatohepatitis （NASH） and progressive liver disease including cirrhosis and hepatocellular carcinoma. A growing body of ... Nonalcoholic fatty liver disease （NAFLD） is highly prevalent and can result in nonalcoholic steatohepatitis （NASH） and progressive liver disease including cirrhosis and hepatocellular carcinoma. A growing body of literature implicates the peroxisome proliferators- activated receptors （PPARs） in the pathogenesis and treatment of NAFLD. These nuclear hormone receptors impact on hepatic triglyceride accumulation and insulin resistance. The aim of this review is to describe the data linking PPARα and PPART to NAFLD/NASH and to discuss the use of PPAR ligands for the treatment of NASH. 展开更多
关键词 Non-alcoholic fatty liver disease Peroxisome proliferators-activated receptors Insulin resiatance Metabolic syndrome Pharmacologic ligands
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Troglitazone,a peroxisome proliferator-activated receptorγligand,induces growth inhibition and apoptosis of HepG2 human liver cancer cells 认领 引用 被引量：10
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作者 Yan-Ming Zhou Yin-Hao Wen +3 位作者 Xiao-Yan Kang Hai-Hua Qian Jia-Mei Yang Zheng-Feng Yin 《World Journal of Gastroenterology》 SCIE CAS 2008年第14期2168-2173,共6页
AIM:To examine the effect of troglitazone,a peroxisome proliferator-activated receptorγ(PPARγ)ligand,on the proliferation and apoptosis of human liver cancer cells.METHODS:Liver cancer cell line HepG2 was cultured a... AIM:To examine the effect of troglitazone,a peroxisome proliferator-activated receptorγ(PPARγ)ligand,on the proliferation and apoptosis of human liver cancer cells.METHODS:Liver cancer cell line HepG2 was cultured and treated with troglitazone.Cell proliferation was detected by 3-(4-,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide(MTT)assay;apoptosis was detected by flow cytometry and terminal deoxynucleotidyl transferase-mediated nick end labeling of DNA fragmentation sites(TUNEL)assay;and apoptosis-related protein was detected by immunocytochemistry and Western blotting.RESULTS:Troglitazone inhibited growth and induced apoptosis of HepG2 cells in a dose-dependent manner,and induced activation of caspase-3 expression.Troglitazone not only drove apoptosis-inhibiting factor survivin to translocate incompletely from the nucleus to the cytoplasm,but also inhibited expression of survivin,while it did not affect expression of apoptosis-promoting factor Bax.CONCLUSION:PPARγligands inhibit growth and induce apoptosis of liver cancer cells,and may have applications for the prevention and treatment of liver cancer. 展开更多
关键词 Peroxisome proliferator-activated receptorγ Troglitazone Liver neoplasms Apoptosis
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Peroxisome proliferator-activated receptor γ agonist reduces the severity of post-ERCP pancreatitis in rats 认领 引用 被引量：7
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作者 Emma Folch-Puy Susana Granell +2 位作者 Juan L Iovanna Marc Barthet Daniel Closa 《World Journal of Gastroenterology》 SCIE CAS 2006年第40期6458-6463,共6页
AIM： To determine the effects of prophylactic peroxisome proliferator-activated receptor （PPARy） agonist administration in an experimental model of post-endoscopic retrograde cholangiopancreatography （post-ERCP） ... AIM： To determine the effects of prophylactic peroxisome proliferator-activated receptor （PPARy） agonist administration in an experimental model of post-endoscopic retrograde cholangiopancreatography （post-ERCP） acute pancreatitis. METHODS： Post-ERCP pancreatitis was induced in male Wistar rats by infusion of contrast medium into the pancreatic duct. In additional group, rosiglitazone, a PPARγ agonist, was administered 1 h before infusion of contrast medium. Plasma and pancreas samples were obtained 6 h after the infusion. RESULTS： Infusion of contrast medium into the pancreatic duct resulted in an inflammatory process characterized by increased lipase levels in plasma, and edema and myeloperoxidase activity （MPO） in pancreas. This result correlated with the activation of nuclear factor κB （NFκB） and the inducible NO synthase （iNOS） expression in pancreatic cells. Rosiglitazone reduced the increase in lipase and the level of edema and the increase in myeloperoxidase as well as the activation of NFκB and iNOS expression. CONCLUSION： A single oral dose of rosiglitazone, given 1 h before post-ERCP pancreatitis induction is effective in reducing the severity of the subsequent inflammatory process. The protective effect of rosiglitazone was associated with NFκB inhibition and the blockage of leukocyte infiltration in pancreas. 展开更多
关键词 Peroxisome proliferator-activated receptor γ Pancreatitis Endoscopic retrograde cholangio pancreatography Inflammation Nuclear factor κB
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Peroxisome proliferator-activated receptor α,a potential therapeutic target for alcoholic liver disease 认领 引用 被引量：19
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作者 Yue-Min Nan Rong-Qi Wang Na Fu 《World Journal of Gastroenterology》 SCIE CAS 2014年第25期8055-8060,共6页
Alcoholic liver injury represents a progressive process with a range of consequences including hepatic steatosis, steatohepatitis, liver fibrosis, cirrhosis, and hepatocellular carcinoma. Targeting key molecular regul... Alcoholic liver injury represents a progressive process with a range of consequences including hepatic steatosis, steatohepatitis, liver fibrosis, cirrhosis, and hepatocellular carcinoma. Targeting key molecular regulators involved in the development of alcoholic liver injury may be of great value in the prevention of liver injury. Peroxisome proliferator-activated receptor &#x003b1; (PPAR&#x003b1;) plays a pivotal role in modulation of hepatic lipid metabolism, oxidative stress, inflammatory response and fibrogenesis. As such, PPAR&#x003b1; may be a potential therapeutic target for the treatment of alcoholic liver disease. 展开更多
关键词 Alcoholic liver disease Oxidative stress Inflammation Fibrosis Peroxisome proliferator-activated receptor α
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EFFECT OF PEROXISOME PROLIFERATOR-ACTIVATED RECEPTOR ACTIVATORS ON TUMOR NECROSIS FACTOR-αEXPRESSION IN NEONATAL RAT CARDIAC MYOCYTES 认领 引用 被引量：7
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作者 Ping Ye Hong Fang +2 位作者 Xin Zhou Yan-li He Yong-xue Liu 《Chinese Medical Sciences Journal》 CAS 2004年第4期243-247,共5页
Objective To investigate the effect of peroxisome proliferator-activated receptor-α(PPARα)and PPARγactivators on tumor necrosis factor-α(TNFα)expression in neonatal rat cardiac myocytes.Methods Primary cultures o... Objective To investigate the effect of peroxisome proliferator-activated receptor-α(PPARα)and PPARγactivators on tumor necrosis factor-α(TNFα)expression in neonatal rat cardiac myocytes.Methods Primary cultures of cardiac myocytes from 1-to 3-day-old Wistar rats were prepared,and myocytes were ex-posed to lipopolysaccharide(LPS)and varying concentrations of PPARαor PPARγactivator(fenofibrate or pioglitazone).RT-PCR and ELISA were used to measure TNFα,PPARα,and PPARγexpression in cultured cardiac myocytes.Transient tr-ansfection of TNFαpromoter with or without nuclear factor-kappaB(NF-κB)binding site to cardiac myocytes was performed.Results Pretreatment of cardiac myocytes with fenofibrate or pioglitazone inhibited LPS-induced TNFαmRNA and protein expression in a dose-dependent manner.However,no significant changes were observed on PPARαor PPARγmRNA expression when cardiac myocytes were pretreated with fenofibrate or pioglitazone.Proportional suppression of TNFαpromoter activity was observed when myocytes was transiently transfected with whole length of TNFαpromoter(-721/+17)after being stimulated with LPS and fenofibrate or pioglitazone,whereas no change of promoter activity was observed with transfection of TNFαreporter construct in deletion of NF-κB binding site(-182/+17).Conclusions PPARαand PPARγactivators may inhibit cardiac TNFαexpression but not accompanied by change of PPARαor PPARγmRNA expression.Therefore PPARαand PPARγactivators appear to play a role in anti-inflammation.The mechanism may partly be involved in suppression of the NF-κB pathway. 展开更多
关键词 peroxisome proliferator-activated receptors tumor necrosis factor-a cardiac myocytes activators
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Peroxisome proliferator-activated receptor-γ is essential in the pathogenesis of gastric carcinoma 认领 引用 被引量：13
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作者 Xiu-Mei Ma Hong Yu Na Huai 《World Journal of Gastroenterology》 SCIE CAS 2009年第31期3874-3883,共10页
AIM： To investigate whether peroxisome proliferatoractivated receptor γ （PPAR-γ） is expressed in human gastric carcinoma and whether PPAR-γ, is a potential target for gastric carcinoma therapy. METHODS： PPAR-γ... AIM： To investigate whether peroxisome proliferatoractivated receptor γ （PPAR-γ） is expressed in human gastric carcinoma and whether PPAR-γ, is a potential target for gastric carcinoma therapy. METHODS： PPAR-γ protein in gastric carcinoma was examined by immunohistochemistry. In the gastric carcinoma cell line MGCS03, PPAR-7, survivin, Skp2 and p27 protein and mRNA were examined by Western blotting and real-time reverse transcription-polymerase chain reaction, respectively; proliferation was examined by MTT; apoptosis was examined by chromatin staining with Hoechst 33342 and fluorescence activated cell sorting （FACS）. and cell cycle was examined by FACS; the knockdown of PPAR-γ was done by RNA interference. RESULTS： A high level of expression of PPAR-γ was observed in human gastric carcinoma and in a human gastric carcinoma cell line MGCS03. The PPAR-γ agonist 15-deoxy-△12,14-prostaglandin J2 （15d-PGJ2）inhibited growth, and induced apoptosis and G1/G0 cell cycle arrest in MGC803 cells in a concentration-dependent and time-dependent manner. The effect of 15d-PGJ2 on MGC803 cells was not reversed by the selective and irreversible antagonist GW9662 for PPAR-γ. Furthermore, survivin and Skp2 expression were decreased, whereas p27 expression was enhanced following 15d-PGJ2 treatment in a dose-dependent manner in MGC803 cells. Interestingly, we also found that small interfering RNA for PPAR-γ inhibited growth and induced apoptosis in MGC803 cells. The inhibition of PPAR-γ function may be a potentially important and novel modality for treatment and prevention of gastric carcinoma. CONCLUSION： A PPAR-γ agonist inhibited growth of human gastric carcinoma MGC803 cells by inducing apoptosis and G1/G0 cell cycle arrest with the involvement of survivin, Skp2 and p27 and not via PPAR-γ. 展开更多
关键词 Peroxisome proliferator-activated receptor Gastric cancer Apoptosis Cell cycle
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Suppression of pancreatic carcinoma growth by activating peroxisome proliferator-activated receptor γ involves angiogenesis inhibition 认领 引用 被引量：14
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作者 Yu-Wei Dong Xing-Peng Wang Kai Wu 《World Journal of Gastroenterology》 SCIE CAS 2009年第4期441-448,共8页
AIM： TO Study the possible actions and mechanisms or peroxisome proliferator-activated receptor γ （PPARγ）, a ligand-activated transcription factor, in pancreatic car- cinogenesis, especially in angiogenesis. METH... AIM： TO Study the possible actions and mechanisms or peroxisome proliferator-activated receptor γ （PPARγ）, a ligand-activated transcription factor, in pancreatic car- cinogenesis, especially in angiogenesis. METHODS： Expressions of PPARy and retinoid acid receptor （RXRα） were examined by reverse-transcription polymerase chain reaction （RT-PCR） with immunocyto- chemical staining. Pancreatic carcinoma cells, PANC-1, were treated either with 9-cis-RA, a ligand of RXRα, or with 15-deoxy-△12,14 prostaglandin J2 （15d-PGJ2）, a ligand of PPART, or both. Antiproliferative effect was evaluated by cell viability using methyltetrazolium （MTT） assay. A pancreatic carcinoma xenograft tumor model of nude mice was established by inoculating PANC-1 cells subcutaneously. Rosiglitazone, a specific ligand of PPARy, was administered via water drinking in experimental group of nude mice. After 75 d, all mice were sacrificed. Expression of proliferating cell nuclear antigen （PCNA） in tumor tissue was examined with immunohistochemical staining. Expression of vascular endothelial growth factor （VEGF） mRNA in PANC-1 cells, which were treated with 15d-PGJ2 or 9-cis-RA at various concentrations or different duration, was detected by semi-quantitative RT-PCR. Effects of Rosi- glitazone on changes of microvascular density （MVD） and VEGF expression were investigated in xenograft tumor tissue. Neovasculature was detected with immu- nohistochemistry staining labeled with anti-Ⅳ collagen antibody, and indicated by MVD. RESULTS： RT-PCR and immunocytochemical stain- ing showed that PPARγ and RXRα were expressed in PANC-1 cells at both transcription level and translation level. MTT assay demonstrated that 15d-PGJ2, 9-cis-RA and their combination inhibited the growth of PANC-1 cells in a dose-dependent manner. 9-cis-RA had a com- bined inhibiting action with 15d-PGJ2 on the growth of pancreatic carcinoma. In vivo studies revealed that Rosiglitazone significantly suppressed the growth of pancreatic carcinoma as compared to control group （0.48 ± 0.23 cm^3 vs 2.488 ± 0.59 cm^3, P 〈 0.05）, and the growth inhibition rate was 80.7%. Immuno- histochemistry study showed that PCNA was down regulated in Rosiglitazone-treated group compared to the control group. 15d-PGJ2, 9-cis-RA and their com- bination inhibited the expression of VEGF mRNA in PANC-1 cells in a dose- and time-dependent manner. MVD was decreased more significantly in Rosiglitazone- treated mice （10.67±3.07） than in the control group （31.44±6.06） （P 〈 0.01）. VEGF expression in xeno- graft tumor tissue was also markedly down-regulated in Rosiglitazone-treated mice. CONCLUSION： Activation of PPARγ, inhibits the growth of pancreatic carcinoma both in vitro and in vivo. Sup- pression of tumor angiogenesis by down-regulating the expression of VEGF may be one of the mechanisms by which PPARγ, activation inhibits the growth of pancre- atic carcinoma. 展开更多
关键词 Pancreatic carcinoma Peroxisome prolifer-ator-activated receptor γ Angiogenesis Vascular en-dothelial growth factor
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Construction and Evaluation of Merged Pharmacophore Based on Peroxisome Proliferator Receptor-Alpha Agonists 认领 引用 被引量：4
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作者 Lian-sheng Qiao Yu-su He +5 位作者 Xiao-qian Huo Lu-di Jiang Yan-kun Chen Xi Chen Yan-ling Zhang Gong-yu Li 《Chinese Journal of Chemical Physics》 SCIE EI CAS CSCD 2016年第4期508-516,I0002,共9页
Pharmacophore is a commonly used method for molecular simulation,including ligand-based pharmacophore(LBP)and structure-based pharmacophore(SBP).LBP can be utilized to identify active compounds usual with lower accura... Pharmacophore is a commonly used method for molecular simulation,including ligand-based pharmacophore(LBP)and structure-based pharmacophore(SBP).LBP can be utilized to identify active compounds usual with lower accuracy,and SBP is able to use for distin-guishing active compounds from inactive compounds with frequently higher missing rates.Merged pharmacophore(MP)is presented to integrate advantages and avoid shortcomings of LBP and SBP.In this work,LBP and SBP models were constructed for the study of per-oxisome proliferator receptor-alpha(PPARα)agonists.According to the comparison of the two types of pharmacophore models,mainly and secondarily pharmacological features were identified.The weight and tolerance values of these pharmacological features were adjusted to construct MP models by single-factor explorations and orthogonal experimental design based on SBP model.Then,the reliability and screening efficiency of the best MP model were validated by three databases.The best MP model was utilized to compute PPARαactivity of compounds from traditional Chinese medicine.The screening efficiency of MP model outperformed individual LBP or SBP model for PPARαagonists,and was similar to combinatorial screening of LBP and SBP.However,MP model might have an advantage over the combination of LBP and SBP in evaluating the activity of compounds and avoiding the inconsistent prediction of LBP and SBP,which would be beneficial to guide drug design and optimization. 展开更多
关键词 Merged pharmacophore Ligand-based pharmacophore Structure-based pharmaeophore Peroxisome proliferator receptor-alpha Docking Combinatorial screening
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Decreased hepatic peroxisome proliferator-activated receptor-γ contributes to increased sensitivity to endotoxin in obstructive jaundice 认领 引用 被引量：4
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作者 Xin Lv Jian-Gang Song +5 位作者 Hong-Hai Li Jun-Ping Ao Ping Zhang Ye-Sheng Li Shao-Li Song Xiang-Rui Wang 《World Journal of Gastroenterology》 SCIE CAS CSCD 2011年第48期5267-5273,共7页
AIM: To investigate the role of hepatic peroxisome proliferator-activated receptor-γ (PPAR-γ) in increased susceptibility to endotoxin-induced toxicity in rats with bile duct ligation during endotoxemia.METHODS: Mal... AIM: To investigate the role of hepatic peroxisome proliferator-activated receptor-γ (PPAR-γ) in increased susceptibility to endotoxin-induced toxicity in rats with bile duct ligation during endotoxemia.METHODS: Male Sprague-Dawley rats were subjected to bile duct ligation (BDL). Sham-operated animals served as controls. DNA binding were determined by polymerase chain reaction, Western blotting analysis,and electrophoretic mobility shift assay, respectively.BDL and sham-operated rats received a non-lethal dose of intraperitoneal lipopolysaccharide (LPS) injection (3 mg/kg, i.p.). Additionally, the potential beneficial effects of the PPAR-γ agonist rosiglitazone were determined in BDL and sham-operated rats treated with a non-lethal dose of LPS. Survival was assessed in BDL rats treated with a non-lethal dose of LPS and in sham-operatedrats treated at a lethal dose of LPS (6 mg/kg, i.p.).RESULTS: PPAR-γ activity in rats undergoing BDL wassignificantly lower than in the sham-controls. Hepatic PPAR-γ gene expression was downregulated at both them RNA and protein levels. In a parallel group, serumlevels of pro-inflammatory cytokines were nearly unde-tectable in the sham-operated rats. When challenged with a non-lethal dose of LPS (3 mg/kg), the BDL ratshad approximately a 2.4-fold increase in serum IL-6,a 2.7 fold increase in serum TNF-α, 2.2-fold increasein serum IL-1 and 4.2-fold increase in serum ALT. Thesurvival rate was significantly lower as compared with that in sham-operated group. Additionally, rosiglitazone significantly reduced the concentration of TNF-α, IL-1β, IL-6 and ALT in sham-operated rats, but not in BDL rats, in response to LPS (3 mg/kg). Also, the survival was improved by rosiglita zone in sham-operated rats challenged with a lethal dose of LPS, but not in BDL rats, even with a non-lethal dose of LPS (3 mg/kg).CONCLUSION: Obstructive jaundice downregulates hepatic PPAR-γ expression, which in turn may contributeto hypersensitivity towards endotoxin. 展开更多
关键词 Obstructive jaundice Endotoxemia Liver Peroxisome proliferator-activated receptor-γ Rosiglitazone
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Association of β3 Adrenergic Receptor and Peroxisome Proliferator-activated Receptor Gamma 2 Polymorphisms With Insulin Sensitivity:A Twin Study 认领 引用 被引量：3
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作者 TIAN-JIAO CHEN CHENG-YE JI +1 位作者 XIAO-YING ZHENG AND YONG-HUAHU 《Biomedical and Environmental Sciences》 SCIE CAS 2007年第2期99-105,共7页
Objective To study the effect of β3 adrenergic receptor （β3AR） Trp64Arg and peroxisome proliferator activated receptor gamma 2 （PPAR72） Prol2Ala polymorphisms on insulin resistance. Methods One hundred and eight... Objective To study the effect of β3 adrenergic receptor （β3AR） Trp64Arg and peroxisome proliferator activated receptor gamma 2 （PPAR72） Prol2Ala polymorphisms on insulin resistance. Methods One hundred and eight dizygotic twin pairs were enrolled in this study. Microsatellite polymorphism was used to diagnose zygosity of twins. Insulin sensitivity was estimated with logarithm transformed homeostasis model assessment （HOMA）. PCR-RFLP analysis was performed to detect the variants. As a supplement to the sib-pair method, identity by state （IBS） was used to analyze the association of polymorphisms with insulin sensitivity. Results The genotype frequencies of Trp64Trg, Trp64Arg, and Arg64Arg were 72.3%, 23.8%, and 3.9%, respectively, while the genotype frequencies of Pro12Pro, Pro12Ala, and Ala12Ala were 89.9%, 9.6%, and 0.5%, respectively. For β3AR Trp64Arg the interclass co-twin correlations of Waist-to-hip ratio （WHR）, blood glucose （GLU）, and insulin （INS）, homeostasis model assessment insulin resistance index （HOMA-IR） of the twin pairs sharing 2 alleles of IBS were greater than those sharing 0-1 allele of IBS, and HOMA4R had statistic significance. For PPAR3t2 Prol2Ala most traits of twin pairs sharing 2 alleles of IBS had greater correlations and statistic significance in body mass index （BMI）, WHR, percent of body fat （PBF） and GLU, but there were low correlations of either insulin or HOMA-IR of twin pairs sharing 1 or 2 alleles of IBS. The combined effects of the two variations showed less squared significant twin-pair differences of INS and HOMA-IR among twins sharing 4 alleles of IBS. Condusions β3AR Trp64Arg and PPAR）,2 Pro 12Ala polymorphisms might be associated with insulin resistance and obesity, and there might be slight synergistic effects between this two gene loci, and further studies are necessary to confirm this finding. 展开更多
关键词 Dizygotic twins Beta-3 adrenergic receptor Peroxisome proliferator activated receptor gamma 2 Polymorphism Insulin resistance.
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THE INCREASE IN PLASMINOGEN ACTIVATOR INHIBITOR TYPE-1 EXPRESSION BY STIMULATION OF ACTIVATORS FOR PEROXISOME PROLIFERATOR-ACTIVATED RECEPTORS IN HUMAN ENDOTHELIAL CELLS 认领 引用 被引量：5
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作者 叶平 胡晓晖 赵亚力 《Chinese Medical Sciences Journal》 CAS 2002年第2期112-116,共5页
Objective.To investigate the effect of peroxis ome proliferator-activated recept ors(PPARs )activators on plasminogen activator inhibitor ty pe-1(PAI-1)expression in human umbilical vein e ndothelial cells and the pos... Objective.To investigate the effect of peroxis ome proliferator-activated recept ors(PPARs )activators on plasminogen activator inhibitor ty pe-1(PAI-1)expression in human umbilical vein e ndothelial cells and the possi-ble mechanism.Methods.Human umbilical vein endothelial ce lls(HUVECs )were obtained from normal fetus,and cul-tured conventionally.Then the HUVECs were exposed to test agents(linolenic acid,linoleic acid,oleic acid,stearic acid and prostaglandin J 2 respectively)in varying concentrations with fresh media.RT -PCR and ELISA were applied to determine the expression of PPARs and PAI-1in HUVECs.Results.PPARα,PPARδand PPARγmRNA were detected by using RT-PCR in HUVECs.Treatment of HUVECs with PPARαand PPARγactivators---linolenic acid,linoleic acid,oleic acid and prostaglandin J 2 respectively,but not with stearic a cid could augment PAI-I mRNA expression and protein secretion in a concentration-dependent manner.However,the mRNA expressions of 3subclasses of PPAR with their activators in HUVECs were not changed compared w ith controls.Conclusion.HUVECs express PPARs.PPARs activators may increase PAI-1expression in ECs,but the underlying mechanism remains uncle ar.Although PPARs expression was not enhanced after stimulated by their activators in ECs,the role of functionally active PPARs in regulating PA I-1expression in ECs needs to be further investigated by using transient gen e transfection assay. 展开更多
关键词 peroxisome proliferator-activate d receptors plasminogen activator inhibitor type-1 expression endothelial cells
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Peroxisome proliferator-activated receptors for hypertension 认领 引用 被引量：20
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作者 Daisuke Usuda Tsugiyasu Kanda 《World Journal of Cardiology》 2014年第8期744-754,共11页
Peroxisome proliferator-activated receptors(PPARs) are ligand-activated transcription factors belonging to the nuclear receptor superfamily, which is composed of four members encoded by distinct genes(α, β, γ, and ... Peroxisome proliferator-activated receptors(PPARs) are ligand-activated transcription factors belonging to the nuclear receptor superfamily, which is composed of four members encoded by distinct genes(α, β, γ, and δ). The genes undergo transactivation or transrepression under specific mechanisms that lead to the induction or repression of target gene expression. As is the case with other nuclear receptors, all four PPAR isoforms contain five or six structural regions in four functional domains; namely, A/B, C, D, and E/F. PPARs have many functions, particularly functions involving control of vascular tone, inflammation, and energy homeostasis, and are, therefore, important targets for hypertension, obesity, obesity-induced inflammation, and metabolic syndrome in general. Hence, PPARs also represent drug targets, and PPARα and PPARγ agonists are used clinically in the treatment of dyslipidemia and type 2 diabetes mellitus, respectively. Because of their pleiotropic effects, they have been identified as active in a number of diseases and are targets for the development of a broad range of therapies for a variety of diseases. It is likely that the range of PPARγ agonist therapeutic actions will result in novel approaches to lifestyle and other diseases. The combination of PPARs with reagents or with other cardiovascular drugs, such as diuretics and angiotensin Ⅱ receptor blockers, should be studied.This article provides a review of PPAR isoform characteristics, a discussion of progress in our understanding of the biological actions of PPARs, and a summary of PPAR agonist development for patient management. We also include a summary of the experimental and clinical evidence obtained from animal studies and clinical trials conducted to evaluate the usefulness and effectiveness of PPAR agonists in the treatment of lifestyle-related diseases. 展开更多
关键词 Peroxisome proliferator-activated receptors Nuclear receptor Isoform mRNA Blood pressure Hypertension Obesity Angiotensin II receptor blocker Diabetes mellitus
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Leptin and peroxisome proliferator-activated receptor γ expression in colorectal adenoma 认领 引用 被引量：2
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作者 Hyung Hun Kim You Sun Kim +1 位作者 Yun Kyung Kang Jeong Seop Moon 《World Journal of Gastroenterology》 SCIE CAS CSCD 2012年第6期557-562,共6页
AIM： To investigate the expressions of leptin and per- oxisome proliferator-activated receptor y （PPARG） in relation to body mass index （BMI）. METHODS： We evaluated leptin and PPARG expres- sion in 30 adenomas o... AIM： To investigate the expressions of leptin and per- oxisome proliferator-activated receptor y （PPARG） in relation to body mass index （BMI）. METHODS： We evaluated leptin and PPARG expres- sion in 30 adenomas over 1 cm in size by immunohisto- chemical staining. In addition, clinicopathologic features including BMI were assessed. RESULTS： PPARG and leptin expression showed a strong positive correlation （P = 0.035）. The average BMI of the leptin-positive group was higher than that of the leptin-negative group （25.4 ＋ 3.4 kg/m2 vs 22.6 ＋ 2.4 kg/m2, P = 0.018）, and leptin expression was sig- nificantly correlated with high BMI （P = 0.024）. Leptinexpression was more frequently observed in intermedi- ate/high grade dysplasia than in low grade dysplasia （P = 0.030）. However, PPARG expression was not cor- related with BMI and grade of dysplasia. CONCLUSION： BMI has influenced on the leptin ex- pression of colorectal adenoma. The exact mechanism underlies the strong correlation between leptin and PPARG expression needs further study. 展开更多
关键词 Leptin Peroxisome proliferator-activated re-ceptor y Obesity Body mass index Colorectal adenoma
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