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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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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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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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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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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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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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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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Peroxisome proliferator-activated receptor gamma as a therapeutic target for hepatocellular carcinoma:Experimental and clinical scenarios 认领 引用 被引量：3
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作者 Swati Katoch Vinesh Sharma Vikram Patial 《World Journal of Gastroenterology》 SCIE CAS 2022年第28期3535-3554,共20页
Hepatocellular carcinoma(HCC)is the most common type of liver cancer worldwide.Viral hepatitis is a significant risk factor for HCC,although metabolic syndrome and diabetes are more frequently associated with the HCC.... Hepatocellular carcinoma(HCC)is the most common type of liver cancer worldwide.Viral hepatitis is a significant risk factor for HCC,although metabolic syndrome and diabetes are more frequently associated with the HCC.With increasing prevalence,there is expected to be>1 million cases annually by 2025.Therefore,there is an urgent need to establish potential therapeutic targets to cure this disease.Peroxisome-proliferator-activated receptor gamma(PPARγ)is a ligand-activated transcription factor that plays a crucial role in the pathophysiology of HCC.Many synthetic agonists of PPARγsuppress HCC in experimental studies and clinical trials.These synthetic agonists have shown promising results by inducing cell cycle arrest and apoptosis in HCC cells and preventing the invasion and metastasis of HCC.However,some synthetic agonists also pose severe side effects in addition to their therapeutic efficacy.Thus natural PPARγagonists can be an alternative to exploit this potential target for HCC treatment.In this review,the regulatory role of PPARγin the pathogenesis of HCC is elucidated.Furthermore,the experimental and clinical scenario of both synthetic and natural PPARγagonists against HCC is discussed.Most of the available literature advocates PPARγas a potential therapeutic target for the treatment of HCC. 展开更多
关键词 Anticancer Hepatocellular carcinoma Natural agonists Peroxisome proliferator-activated receptor-γ Thiazolidinediones
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Peroxisome proliferator-activated receptor γ and colorectal cancer 认领 引用 被引量：6
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作者 Yun Dai Wei-Hong Wang 《World Journal of Gastrointestinal Oncology》 SCIE 2010年第3期159-164,共6页
Peroxisome proliferator-activated receptors(PPARs) are members of the nuclear hormone receptor superfamily and ligand-activated transcription factors.PPARγ plays an important role in adipocyte differentiation,lipid s... Peroxisome proliferator-activated receptors(PPARs) are members of the nuclear hormone receptor superfamily and ligand-activated transcription factors.PPARγ plays an important role in adipocyte differentiation,lipid storage and energy dissipation in adipose tissue,and is involved in the control of inflammatory reactions as well as in glucose metabolism through the improvement of insulin sensitivity.Growing evidence has demonstrated that activation of PPARγ has an antineoplastic effect in tumors,including colorectal cancer.High expression of PPARγ is detected in human colon cancer cell lines and adenocarcinoma.This review describes the molecular mechanisms by which PPARγ regulates tumorigenesis in colorectal cancer,and examines current clinical trials evaluating PPARγ agonists as therapeutic agents for colorectal cancer. 展开更多
关键词 Colorectal cancer Peroxisome proliferator-activated receptors Ligand Tumor suppression
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Peroxisome proliferator-activated receptors as targets to treat non-alcoholic fatty liver disease 认领 引用 被引量：22
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作者 Vanessa Souza-Mello 《World Journal of Hepatology》 2015年第8期1012-1019,共8页
Lately, the world has faced tremendous progress in the understanding of non-alcoholic fatty liver disease(NAFLD) pathogenesis due to rising obesity rates. Peroxisome proliferator-activated receptors(PPARs) are transcr... Lately, the world has faced tremendous progress in the understanding of non-alcoholic fatty liver disease(NAFLD) pathogenesis due to rising obesity rates. Peroxisome proliferator-activated receptors(PPARs) are transcription factors that modulate the expression of genes involved in lipid metabolism, energy homeostasis and inflammation, being altered in diet-induced obesity. Experimental evidences show that PPAR-alpha is the master regulator of hepatic beta-oxidation(mitochondrial and peroxisomal)and microsomal omega-oxidation, being markedly decreased by high-fat(HF) intake. PPAR-beta/delta is crucial to the regulation of forkhead box-containing protein O subfamily-1 expression and, hence, the modulation of enzymes that trigger hepatic gluconeogenesis. In addition, PPAR-beta/delta can activate hepatic stellate cells aiming to the hepatic recovery from chronic insult. On the contrary, PPAR-gamma upregulation by HF diets maximizes NAFLD through the induction of lipogenic factors, which are implicated in the fatty acid synthesis. Excessive dietary sugars also upregulate PPAR-gamma, triggering de novo lipogenesis and the consequent lipid droplets deposition within hepatocytes. Targeting PPARs to treat NAFLD seems a fruitful approach as PPAR-alpha agonist elicits expressive decrease in hepatic steatosis by increasing mitochondrial beta-oxidation, besides reduced lipogenesis. PPAR-beta/delta ameliorates hepatic insulin resistance by decreasing hepatic gluconeogenesis at postprandial stage. Total PPAR-gamma activation can exert noxious effects by stimulating hepatic lipogenesis. However, partial PPAR-gamma activation leads to benefits, mainly mediated by increased adiponectin expression and decreased insulin resistance. Further studies are necessary aiming at translational approaches useful to treat NAFLD in humans worldwide by targeting PPARs. 展开更多
关键词 Peroxisome proliferator-activated receptors Non-alcoholic fatty liver disease Obesity Treatment Insulin resistance Beta-oxidation Lipogenesis
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Expression for peroxisome proliferator-activated receptor gamma in pituitary adenomas 38 cases for semi-quantitative immunohistochemical analysis 认领 引用 被引量：1
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作者 Xiaojie Lu Kailai Chen +4 位作者 Weiyang Ji Qing Wang Bing Li Jiang'an Li Jiyong Sun 《Neural Regeneration Research》 SCIE CAS 2008年第7期756-759,共4页
BACKGROUND:It has been reported that peroxisome proliferator-activated receptorγ(PPARγ)is highly expressed in lung cancer,colon cancer,and gastric cancer,as well as other tumors.OBJECTIVE:To study expression of PPAR... BACKGROUND:It has been reported that peroxisome proliferator-activated receptorγ(PPARγ)is highly expressed in lung cancer,colon cancer,and gastric cancer,as well as other tumors.OBJECTIVE:To study expression of PPARγin pituitary adenomas and analyze the role of PPARγin hormonal typing of pituitary adenomas.DESIGN,TIME AND SETTING:Semi-quantitative immunohistochemistry of pathological specimens.The experiment was conducted at the Department of Neurosurgery,Wuxi Second Hospital Affiliated to Nanjing Medical University between January 2002 and May 2005.MATERIALS:Surgical resection samples of pituitary adenomas from 38 cases(18 male and 20 female)were analyzed.Eight cases were determined to be invasive pituitary adenomas and 30 cases were non-invasive pituitary adenomas.Hormonal classification of the types of pituitary adenomas revealed somatotrophic adenomas in six cases,corticotrophic adenoma in five cases,prolactinomas in 13 cases,multi-hormone secreting adenomas in six cases,and eight cases of adenoma without altered endocrine function.Five autopsy specimens were collected during the same period from patients of matching age that died from unrelated diseases and were included as normal anterior pituitar3,controls.METHODS:Cell counts for positive immunohistochemical signals were recorded from histopathological sections.The percentage of positive cells was reported as a semi-quantitative analysis.MAIN OUTCOME MEASURES:The rate of PPARγpositive cells in different types of adenoma was based on hormonal levels and invasiveness of pituitary tumor cells.RESULTS:All tumor biopsies were determined to express PPARγ.The rate of PPARγ-positive cells ranged between 8%-65%in the pituitary adenomas.According to hormonal type,PPARγexpression did not vary between the groups.In addition,there was no significant difference in PPARγexpression between the non-invasive and invasive pituitary adenomas.CONCLUSIONS:Human pituitary adenomas express PPARγ,and this expression is unrelated to hormonal type and invasiveness. 展开更多
关键词 Peroxisome proliferator-activated receptorγ pituitary adenomas immunohistochemistry
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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 ligand of peroxisome proliferator-activated receptor γ on the biological characters of hepatic stellate cells 认领 引用 被引量：8
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作者 Yan-Tong Guo Xi-Sheng Leng Tao Li Ji-Run Peng Sheng-Han Song Liang-Fa Xiong Zhi-Zhong Qin 《World Journal of Gastroenterology》 SCIE CAS 2005年第30期4735-4739,共5页
AIM： To study the effect of rosiglitazone, which is a ligand of peroxisome proliferator-activated receptor gamma （PPARy）, on the expression of PPARy in hepatic stellate cells （HSCs） and on the biological characte... AIM： To study the effect of rosiglitazone, which is a ligand of peroxisome proliferator-activated receptor gamma （PPARy）, on the expression of PPARy in hepatic stellate cells （HSCs） and on the biological characteristics of HSCs. METHODS： The activated HSCs were divided into three groups： control group, 3 μmol/L rosiglitazone group, and 10 μmol/L rosiglitazone group. The expression of PPARγ, α-smooth muscle actin （α-SMA）, and type Ⅰ and Ⅲ collagen was detected by RT-PCR, Western blot and immunocytochemical staining, respectively. Cell proliferation was determined with methylthiazolyltetrazolium （MTT） colodmetric assay. Cell apoptosis was demonstrated with flow cytometry. RESULTS： The expression of PPARγ at mRNA and protein level markedly increased in HSCs of 10 μmol/L rosiglitazone group （tvalue was 10.870 and 4.627 respectively, P〈0.01 in both）. The proliferation of HSCs in 10 μmol/L rosiglitazone group decreased significantly （t = 5.542, P〈0.01）, α-SMA expression level and type Ⅰ collagen synthesis ability were also reduced VS controls （tvalue = 10.256 and 14.627 respectively, P〈0.01 in both）. The apoptotic rate of HSCs significantly increased in 10 μmol/L rosiglitazone group vs control （X^2= 16.682, P〈0.01）. CONCLUSION： By increasing expression of PPARγ in activated HSCs, rosiglitazone, an agonist of PPARγ, decreases α-SNA expression and type Ⅰ collagen synthesis, inhibits cell proliferation, and induces cell apoptosis. 展开更多
关键词 Peroxisome proliferator-activated receptor gamma Hepatic stellate cell Rosiglitazone
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An innovative approach for the treatment of Alzheimer's disease: the role of peroxisome proliferator-activated receptors and their ligands in development of alternative therapeutic interventions 认领 引用 被引量：3
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作者 Luca Piemontese 《Neural Regeneration Research》 SCIE CAS CSCD 2019年第1期43-45,共3页
Alzheimer＇s disease is a multifactorial pathology, for which no cure is currently available. Nowadays, researchers are moving towards a new hypothesis of the onset of the illness, linking it to a metabolic impairment... Alzheimer＇s disease is a multifactorial pathology, for which no cure is currently available. Nowadays, researchers are moving towards a new hypothesis of the onset of the illness, linking it to a metabolic impairment, q-his innovative approach will lead to the identification of new targets for the preparation of new effective drugs. Peroxisome proliferator-activated receptors and their ligands are the ideal candidates to reach the necessary breakthrough to defeat this complicate disease. 展开更多
关键词 Alzheimer＇s disease multifunctional drugs peroxisome proliferator-activated receptors type 3 diabetes innovative therapies type 2 diabetes mellitus metabolism neuroinflammation
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Peroxisome proliferator-activated receptor agonists:A new hope towards the management of alcoholic liver disease 认领 引用
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作者 Siva Sundara Kumar Durairajan Abhay Kumar Singh Ashok Iyaswamy 《World Journal of Gastroenterology》 SCIE CAS 2024年第35期3965-3971,共7页
In this editorial,we examine a paper by Koizumi et al,on the role of peroxisome proliferator-activated receptor(PPAR)agonists in alcoholic liver disease(ALD).The study determined whether elafibranor protected the inte... In this editorial,we examine a paper by Koizumi et al,on the role of peroxisome proliferator-activated receptor(PPAR)agonists in alcoholic liver disease(ALD).The study determined whether elafibranor protected the intestinal barrier and reduced liver fibrosis in a mouse model of ALD.The study also underlines the role of PPARs in intestinal barrier function and lipid homeostasis,which are both affected by ALD.Effective therapies are necessary for ALD because it is a critical health issue that affects people worldwide.This editorial analyzes the possibility of PPAR agonists as treatments for ALD.As key factors of inflammation and metabolism,PPARs offer multiple methods for managing the complex etiology of ALD.We assess the abilities of PPARα,PPARγ,and PPARβ/δagonists to prevent steatosis,inflammation,and fibrosis due to liver diseases.Recent research carried out in preclinical and clinical settings has shown that PPAR agonists can reduce the severity of liver disease.This editorial discusses the data analyzed and the obstacles,advantages,and mechanisms of action of PPAR agonists for ALD.Further research is needed to understand the efficacy,safety,and mechanisms of PPAR agonists for treating ALD. 展开更多
关键词 Alcoholic liver disease Peroxisome proliferator-activated receptors Peroxisome proliferator-activated receptors agonists Liver fibrosis Inflammation Metabolic regulation Hepatoprotection
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