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Differential activation of Nrf2-Keap1 and NF-kB pathway mediates size-dependent nephrotoxicity of PM0.1,PM2.5,and PM10 particulate matter in mouse model 认领 引用
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作者 Sukhveer Singh Hafsa Hashmi +5 位作者 Neha Singh Priyanka Goswami Pradeep K Singh Mahadeo Kumar Jyotsna Singh Vikas Srivastava 《Journal of Environmental Sciences》 SCIE EI CAS CSCD 2025年第12期179-196,共18页
Air pollution is fourth major cause of death worldwide.Recent evidence suggests that particulate matter(PM)may affect kidneys,and the effect may be size and composition dependent.In this study,PM0.1,PM2.5,and PM... Air pollution is fourth major cause of death worldwide.Recent evidence suggests that particulate matter(PM)may affect kidneys,and the effect may be size and composition dependent.In this study,PM0.1,PM2.5,and PM10were collected from ambient air and given to BALB/c male mice at 0.25 mg/m3 concentration in whole-body inhalation chamber for 28days(6 h/day,5 days/week)to assess their effect on kidney.Physico-chemical characterization of PM particles by SEM,ICP-MS and HPLC showed their various shapes along with the presence of metals and poly aromatic hydrocarbons(PAHs).Following PM exposure,increased serum creatinine levels were observed in animals along with dilated tubules,protein cast deposition,necrosis,immune infiltration,collagen deposition,and shrunken glomeruli in kidney.Immunofluorescence staining showed higher expressions of kidney injury molecule1(KIM-1),cystatin C,β2 microglobulin(β2M),and alpha smooth muscle actin(α-SMA)and fibronectin,suggesting renal injury and fibrosis.PM exposure also increased malondialdehyde(MDA)content and decreased superoxide dismutase 2(SOD2)activity,which in turn leads to induction of inflammation.Mechanistically,PM exposure further inhibited the nuclear factor erythroid 2-related factor 2(Nrf2)signalling and induced kelch-like ECH-associated protein 1(Keap1)and nuclear factor kappa-light-chain-enhancer of activated B(NF-κB).Interestingly,the effect of PM2.5was more severe than PM0.1and PM10,leading to higher levels of proinflammatory NF-κB and greater Nrf2 inhibition.Overall,our findings suggested that inhalation exposure to size-segregated PM can cause kidney damage and fibrosis,and PM2.5showed higher toxicity than PM0.1and PM10. 展开更多
关键词 Particulate Matter(PM0.1 PM2.5and PM10) Nephrotoxicity Kidney fibrosis Inflammation Nrf2-Keap1 NF-κB
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Research on Predicting the Nephrotoxicity Mechanism of Lianqiao-4 Based on Network Pharmacology and Molecular Docking 认领 引用
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作者 Qingchun Bai Gala Bai Huan Wang 《Journal of Clinical and Nursing Research》 2025年第5期89-99,共11页
Objective:To predict the nephrotoxicity mechanism of Lianqiao-4 through network pharmacology and molecular docking methods.Methods:The main chemical components of Lianqiao(Forsythia suspensa),Bistortae rhizoma,Ophiopo... Objective:To predict the nephrotoxicity mechanism of Lianqiao-4 through network pharmacology and molecular docking methods.Methods:The main chemical components of Lianqiao(Forsythia suspensa),Bistortae rhizoma,Ophiopogonis radix,and Clematidis radix et rhizoma,as well as nephrotoxicity-related targets,were screened through databases such as TCMSP,Swiss Target Prediction,GeneCards,and ETCM.Venny 2.1.0 was used to identify the main components of Lianqiao-4 and nephrotoxicity targets.The STRING platform and David database were utilized to construct a protein-protein interaction(PPI)network diagram,while gene function(GO)enrichment analysis and KEGG pathway analysis were conducted.The“Lianqiao-4 active ingredients-nephrotoxicity targets-signaling pathways”network model was constructed using Cytoscape 3.9.1 software.Results:Network pharmacology and molecular docking analysis revealed that the core active ingredients responsible for the nephrotoxicity mechanism of Mongolian medicine Lianqiao-4 include steroidal saponins such as ophiopogonin A,flavonoids like kaempferol and quercetin,steroidal compounds such asβ-sitosterol and sitosterol,and other key regulatory targets including STAT3,ABCG2,HSP90AA1,MMP9,PTGS2,and EGFR.Major pathways involved include lipid and atherosclerosis,chemical carcinogenesis-DNA adducts,and arachidonic acid metabolism.Conclusion:Mongolian medicine Lianqiao-4 exerts its therapeutic effect on nephrotoxicity through multiple components,targets,and pathways,pending experimental verification. 展开更多
关键词 Network pharmacology Molecular docking Lianqiao-4 Nephrotoxicity
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Organic anion transporter 1 and 3 contribute to traditional Chinese medicine-induced nephrotoxicity 认领 引用 被引量：19
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作者 SHEN Qing-Qing WANG Jing-Jing +4 位作者 ROY Debmalya SUN Li-Xin JIANG Zhen-Zhou ZHANG Lu-Yong HUANG Xin 《Chinese Journal of Natural Medicines》 SCIE CAS CSCD 2020年第3期196-205,共10页
With the internationally growing popularity of traditional Chinese medicine(TCM), TCM-induced nephropathy has attracted public attention. Minimizing this toxicity is an important issue for future research. Typical nep... With the internationally growing popularity of traditional Chinese medicine(TCM), TCM-induced nephropathy has attracted public attention. Minimizing this toxicity is an important issue for future research. Typical nephrotoxic TCM drugs such as Aristolochic acid, Tripterygium wilfordii Hook. f, Rheum officinale Baill, and cinnabar mainly damage renal proximal tubules or cause interstitial nephritis. Transporters in renal proximal tubule are believed to be critical in the disposition of xenobiotics. In this review, we provide information on the alteration of renal transporters by nephrotoxic TCMs, which may be helpful for understanding the nephrotoxic mechanism of TCMs and reducing adverse effects. Studies have proven that when administering nephrotoxic TCMs, the expression or function of renal transporters is altered, especially organic anion transporter 1 and 3. The alteration of these transporters may enhance the accumulation of toxic drugs or the dysfunction of endogenous toxins and subsequently sensitize the kidney to injury.Transporters-related drug combination and clinical biomarkers supervision to avoid the risk of future toxicity are proposed. 展开更多
关键词 Traditional Chinese medicine Nephrotoxicity Renal tubular epithelial cell Organic anion transporter Aristolochic acid Tripterygium wilfordii Hook.f. Rheum officinale Baill
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Licorice Extracts Attenuate Nephrotoxicity Induced by Brucine Through Suppression of Mitochondria Apoptotic Pathway and STAT3 Activation 认领 引用 被引量：8
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作者 Min ZHANG Chao WANG +2 位作者 Hua-lin CAI Jing WEN Ping-fei FANG 《Current Medical Science》 SCIE CAS 2019年第6期890-898,共9页
Licorice,one of the most widely used medicinal herbs in East Asia,has effects such as anti-inflammation,antioxidant,and detoxifying.This study aimed to evaluate the protective effect of licorice on brucine-induced nep... Licorice,one of the most widely used medicinal herbs in East Asia,has effects such as anti-inflammation,antioxidant,and detoxifying.This study aimed to evaluate the protective effect of licorice on brucine-induced nephrotoxicity.Sprague Dawley rats were administered with brucine intraperitoneally for 7 consecutive days with or without treatment with licorice.The content of blood urea nitrogen and creatinine in serum,the activities of superoxide dismutase and content of glutathione,malonaldehyde in kidney tissue were detected.Hematoxylin-eosin staining was employed to observe the histopathological changes of kidney.The expression and phosphorylation levels of protein were evaluated by Western blotting and immunohistochemical analysis.The results illustrated that treatment with licorice extracts(LE)significantly protected against the brucineinduced nephrotoxicity by reducing the content of blood urea nitrogen and serum creatinine,attenuating pathologic damage.The unbalance of oxidative stress was repaired by LE via increasing the level of glutathione,promoting the activities of superoxide dismutase and decreasing the content of malonaldehyde.In addition,LE overturned the influence of brucine on apoptosis-related protein and signal transducer and activator of transcription-3(STAT3)activation.Taken together,these data demonstrate that licorice may attenuate brucine-induced nephrotoxicity via inactivation of oxidative stress and mitochondrial-mediated apoptosis pathway.More importantly,the renoprotective effects may be mediated,at least partly,by preventing the activation of STAT3 protein. 展开更多
关键词 licorice brucine nephrotoxicity apoptosis STAT3
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Dual mass spectrometry imaging and spatial metabolomics to investigate the metabolism and nephrotoxicity of nitidine chloride 认领 引用 被引量：5
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作者 Shu Yang Zhonghua Wang +5 位作者 Yanhua Liu Xin Zhang Hang Zhang Zhaoying Wang Zhi Zhou Zeper Abliz 《Journal of Pharmaceutical Analysis》 SCIE CAS CSCD 2024年第7期1011-1023,共13页
Evaluating toxicity and decoding the underlying mechanisms of active compounds are crucial for drug development.In this study,we present an innovative,integrated approach that combines air flowassisted desorption elec... Evaluating toxicity and decoding the underlying mechanisms of active compounds are crucial for drug development.In this study,we present an innovative,integrated approach that combines air flowassisted desorption electrospray ionization mass spectrometry imaging(AFADESI-MSI),time-of-flight secondary ion mass spectrometry(ToF-SIMS),and spatial metabolomics to comprehensively investigate the nephrotoxicity and underlying mechanisms of nitidine chloride(NC),a promising anti-tumor drug candidate.Our quantitive AFADESI-MSI analysis unveiled the region specific of accumulation of NC in the kidney,particularly within the inner cortex(IC)region,following single and repeated dose of NC.High spatial resolution ToF-SIMS analysis further allowed us to precisely map the localization of NC within the renal tubule.Employing spatial metabolomics based on AFADESI-MSI,we identified over 70 discriminating endogenous metabolites associated with chronic NC exposure.These findings suggest the renal tubule as the primary target of NC toxicity and implicate renal transporters(organic cation transporters,multidrug and toxin extrusion,and organic cation transporter 2(OCT2)),metabolic enzymes(protein arginine N-methyltransferase(PRMT)and nitric oxide synthase),mitochondria,oxidative stress,and inflammation in NC-induced nephrotoxicity.This study offers novel insights into NC-induced renal damage,representing a crucial step towards devising strategies to mitigate renal damage caused by this compound. 展开更多
关键词 Nitidine chloride Nephrotoxicity Mass spectrometry imaging Spatial metabolomics Toxicokinetics
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Nephrotoxicity in cancer treatment:An overview 认领 引用 被引量：6
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作者 Maria Luísa Cordeiro Santos Breno Bittencourt de Brito +2 位作者 Filipe Antonio FranÇa da Silva Anelise Costa dos Santos Botelho Fabrício Freire de Melo 《World Journal of Clinical Oncology》 2020年第4期190-204,共15页
Anticancer drug nephrotoxicity is an important and increasing adverse drug event that limits the efficacy of cancer treatment.The kidney is an important elimination pathway for many antineoplastic drugs and their meta... Anticancer drug nephrotoxicity is an important and increasing adverse drug event that limits the efficacy of cancer treatment.The kidney is an important elimination pathway for many antineoplastic drugs and their metabolites,which occurs by glomerular filtration and tubular secretion.Chemotherapeutic agents,both conventional cytotoxic agents and molecularly targeted agents,can affect any segment of the nephron including its microvasculature,leading to many clinical manifestations such as proteinuria,hypertension,electrolyte disturbances,glomerulopathy,acute and chronic interstitial nephritis,acute kidney injury and at times chronic kidney disease.The clinician should be alert to recognize several factors that may maximize renal dysfunction and contribute to the increased incidence of nephrotoxicity associated with these drugs,such as intravascular volume depletion,the associated use of nonchemotherapeutic nephrotoxic drugs(analgesics,antibiotics,proton pump inhibitors,and bonetargeted therapies),radiographic ionic contrast media or radiation therapy,urinary tract obstruction,and intrinsic renal disease.Identification of patients at higher risk for nephrotoxicity may allow the prevention or at least reduction in the development and severity of this adverse effect.Therefore,the aim of this brief review is to provide currently available evidences on oncologic drug-related nephrotoxicity. 展开更多
关键词 Acute kidney injury Cancer Chemotherapy Conventional cytotoxic agents Molecularly targeted agents Nephrotoxicity
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Thyme oil and thymol abrogate doxorubicin-induced nephrotoxicity and cardiotoxicity in Wistar rats via repression of oxidative stress and enhancement of antioxidant defense mechanisms 认领 引用 被引量：4
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作者 Osama M.AHMED Sanaa R.GALALY +1 位作者 Mai RASLAN Mennah-Allah M.A.MOSTAFA 《BIOCELL》 SCIE 2020年第1期41-53,共13页
This study aimed to assess the preventive effects of thyme oil and thymol on doxorubicin(DOX)-induced renotoxicity,cardiotoxicity,and oxidative stress in Wistar rats.Thyme oil was subjected to GC-MS analysis,which ind... This study aimed to assess the preventive effects of thyme oil and thymol on doxorubicin(DOX)-induced renotoxicity,cardiotoxicity,and oxidative stress in Wistar rats.Thyme oil was subjected to GC-MS analysis,which indicated that thymol was the major constituent representing 33.896%.Rats intraperitoneally injected with DOX at a dose of 2 mg/kg b.w./one per week for 7 weeks were co-treated with thyme oil and its major constituent,thymol,at doses 250 and 100 mg/kg b.w./every other day,respectively,by oral gavage for the same period.Thyme oil and thymol markedly ameliorated the raised levels of serum urea,uric acid,and creatinine in DOX-administered rats.They also reduced the elevated activities of serum CK-MB and LDH.Thyme oil was more effective than thymol in decreasing the elevated serum creatinine level and serum CK-MB activity in DOX-administered rats,thereby reflecting its more potent effect on kidney and heart functions.Lipid peroxidation significantly decreased while GSH level and GST and GPx activities significantly increased in kidney and heart of DOX-administered rats treated with thyme oil and thymol.The DOX-induced perturbed kidney histological changes including congestion of glomerulus tuft,inflammatory cells infiltration,protein cast in lumina of the renal tubule,and thickening of the parietal layer of Bowman’s capsule were remarkably ameliorated as a result of treatment with thyme oil and thymol;thyme oil was more effective.In addition,DOX-induced deleterious heart histological alterations,including intramuscular infiltration of inflammatory cells,focal necrosis of cardiac myocytes,and edema,were remarkably reduced by treatment with thyme oil and thymol.Thus,it can be concluded that DOX could induce marked toxicity in kidney and heart,and the treatment with thyme oil or thymol produced potential improvement of kidney and heart function and histological integrity via repression of oxidative stress and enhancement of antioxidant defense mechanisms. 展开更多
关键词 Doxorubicin Nephrotoxicity Cardiotoxicity Oxidative stress Thyme oil Thymol
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Microproteinuria for detecting calcineurin inhibitor-related nephrotoxicity after liver transplantation 认领 引用 被引量：2
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作者 Jing Li Bin Liu +7 位作者 Lu-Nan Yan Lan-Lan Wang Wan Y Lau Bo Li Wen-Tao Wang Ming-Qing Xu Jia-Yin Yang Fu-Gui Li 《World Journal of Gastroenterology》 SCIE CAS 2009年第23期2913-2917,共5页
AIM： To investigate whether microproteinuria could be used as an early and sensitive indicator to detect calcineurin inhibitor （CNI）-related nephrotoxicity after liver transplantation.METHODS： All liver transplant... AIM： To investigate whether microproteinuria could be used as an early and sensitive indicator to detect calcineurin inhibitor （CNI）-related nephrotoxicity after liver transplantation.METHODS： All liver transplant recipients with normal serum creatinine （SCr） and detectable microproteinuria at baseline were included in this study. The renal function was monitored by the blood clearance of 99mTc-diethylenetriaminepentaacetic acid every 6 mo. Microproteinuria, SCr and blood urea nitrogen （BUN） were measured at entry and at subsequent follow-up visits. The patients were divided into different groups according to the mean values of glomerular filtration rate （GFR） at the follow-up time points： Group 1, GFR decreased from baseline by 0%-10%; Group 2, GFR decreased from baseline by 11%-20%; Group 3, GFR decreased from baseline by 21%-40%; Group 4, GFR decreased from baseline by 〉 40% and/or SCr was increasing.RESULTS： A total of 143 patients were enrolled into this study （23 females and 120 males）. The mean follow-up was 32 mo （range 16-36 mo）. Downward trends in renal function over time were observed in the study groups. SCr and BUN increased significantly only in Group 4 patients （P 〈 0.001）. β2-microglobulin （β2m） and al-microglobulin （αlm） significantly increased with the subtle change of renal function in recipients who were exposed to CNI-based immunosuppression regimens. The reductions in GFR were closely correlated with elevated cclm （P = -0.728, P 〈 0.001） and β2m （r2 = -0.787, P 〈 0.001）.CONCLUSION： β2m and α1m could be useful as early and sensitive indicators of CNI-induced nephrotoxicity. 展开更多
关键词 Microproteinuria Liver transplantation Calcineurin inhibitors Nephrotoxicity
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Prevalence of polymyxin-induced nephrotoxicity and its predictors in critically ill adult patients:A meta-analysis 认领 引用 被引量：2
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作者 Jiang-Lin Wang Bi-Xiao Xiang +3 位作者 Xiao-Li Song Rui-Man Que Xiao-Cong Zuo Yue-Liang Xie 《World Journal of Clinical Cases》 SCIE 2022年第31期11466-11485,共20页
BACKGROUND Polymyxin-induced nephrotoxicity is a major safety concern in clinical practice due to long-term adverse outcomes and high mortality.AIM To conducted a systematic review and meta-analysis of the prevalence ... BACKGROUND Polymyxin-induced nephrotoxicity is a major safety concern in clinical practice due to long-term adverse outcomes and high mortality.AIM To conducted a systematic review and meta-analysis of the prevalence and potential predictors of polymyxin-induced nephrotoxicity in adult intensive care unit(ICU)patients.METHODS PubMed,EMBASE,the Cochrane Library and Reference Citation Analysis database were searched for relevant studies from inception through May 30,2022.The pooled prevalence of polymyxin-induced nephrotoxicity and pooled risk ratios of associated factors were analysed using a random-effects or fixed-effects model by Stata SE ver.12.1.Additionally,subgroup analyses and meta-regression were conducted to assess heterogeneity.RESULTS A total of 89 studies involving 12234 critically ill adult patients were included in the meta-analysis.The overall pooled incidence of polymyxin-induced nephrotoxicity was 34.8%.The pooled prevalence of colistin-induced nephrotoxicity was not higher than that of polymyxin B(PMB)-induced nephrotoxicity.The subgroup analyses showed that nephrotoxicity was significantly associated with dosing interval,nephrotoxicity criteria,age,publication year,study quality and sample size,which were confirmed in the univariable meta-regression analysis.Nephrotoxicity was significantly increased when the total daily dose was divided into 2 doses but not 3 or 4 doses.Furthermore,older age,the presence of sepsis or septic shock,hypoalbuminemia,and concomitant vancomycin or vasopressor use were independent risk factors for polymyxin-induced nephrotoxicity,while an elevated baseline glomerular filtration rate was a protective factor against colistin-induced nephrotoxicity.CONCLUSION Our findings indicated that the incidence of polymyxin-induced nephrotoxicity among ICU patients was high.It emphasizes the importance of additional efforts to manage ICU patients receiving polymyxins to decrease the risk of adverse outcomes. 展开更多
关键词 Polymyxins Nephrotoxicity Critically ill adult patients Risk factors Meta-analysis
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Nephroprotective effects of Zingiber zerumbet Smith ethyl acetate extract against paracetamol-induced nephrotoxicity and oxidative stress in rats 认领 引用 被引量：1
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作者 Zariyantey ABDUL HAMID Siti Balkis BUDIN +3 位作者 Ng WEN JIE Asmah HAMID Khairana HUSAIN Jamaludin MOHAMED 《Journal of Zhejiang University-SCIENCE B》 SCIE CAS CSCD 2012年第3期176-185,共10页
Paracetamol (PCM) overdose can cause nephrotoxicity with oxidative stress as one of the possible mechanisms mediating the event. In this study, the effects of ethyl acetate extract of Zingiber zerumbet rhizome [200 mg... Paracetamol (PCM) overdose can cause nephrotoxicity with oxidative stress as one of the possible mechanisms mediating the event. In this study, the effects of ethyl acetate extract of Zingiber zerumbet rhizome [200 mg per kg of body weight (mg/kg) and 400 mg/kg] on PCM-induced nephrotoxicity were examined. Rats were divided into five groups containing 10 rats each. The control group received distilled water while other groups were treated with extract alone (400 mg/kg), PCM alone (750 mg/kg), 750 mg/kg PCM+200 mg/kg extract (PCM+ 200-extract), and 750 mg/kg PCM+400 mg/kg extract (PCM+400-extract), respectively, for seven consecutive days. The Z. zerumbet extract was given intraperitoneally concurrent with oral administration of PCM. Treatment with Z. zerumbet extract at doses of 200 and 400 mg/kg prevented the PCM-induced nephrotoxicity and oxidative impairments of the kidney, as evidenced by a significantly reduced (P<0.05) level of plasma creatinine, plasma and renal malondialdehyde (MDA), plasma protein carbonyl, and renal advanced oxidation protein product (AOPP). Furthermore, both doses were also able to induce a significant increment (P<0.05) of plasma and renal levels of glutathione (GSH) and plasma superoxide dismutase (SOD) activity. The nephroprotective effects of Z. zerumbet extract were confirmed by a reduced intensity of renal cellular damage, as evidenced by histological findings. Moreover, Z. zerumbet extract administered at 400 mg/kg was found to show greater protective effects than that at 200 mg/kg. In conclusion, ethyl acetate extract of Z. zerumbet rhizome has a protective role against PCM-induced nephrotoxicity and the process is probably mediated through its antioxidant properties. 展开更多
关键词 Zingiber zerumbet Antioxidant Oxidative stress Nephrotoxicity Paracetamol
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Melamine Nephrotoxicity is Mediated by Hyperuricemia 认领 引用 被引量：1
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作者 ZHANG Long LI Hong Tian +4 位作者 WANG Lin Lin TRACHTMAN Howard TRASANDE Leonardo WANG Pei Xin LIU Jian Meng 《Biomedical and Environmental Sciences》 SCIE CAS CSCD 2015年第12期904-912,共9页
Objective We tested whether melamine nephrotoxicity was exacerbated by urate(a typical component of renal stones in humans)in rats with hyperuricemiainduced by the uricase inhibitor,potassium oxonate(Oxo).Methods Rats... Objective We tested whether melamine nephrotoxicity was exacerbated by urate(a typical component of renal stones in humans)in rats with hyperuricemiainduced by the uricase inhibitor,potassium oxonate(Oxo).Methods Rats were exposed to melamine or Oxo alone or combinations of melamine(200-400 mg/kg)and Oxo(200-600 mg/kg)for 3 consecutive days.Kidney injury was evaluated by renal biochemical functions,histomorphology,and lipid peroxidation.Kidney crystals were analyzed for their composition.Results Nephrotoxicity was minimal in animals administered melamine or Oxo alone,but it was demonstrable in animals administered at least 800 mg/kg of the two compounds combined.All rats in the 400+600(melamine+Oxo)and 400+400 mg/kg groups and 4 out of 6 in the 200+600 mg/kg group died within 3 days;no rat died in the 200+400 or 200+200 mg/kg group.Dose-dependent renal damage resembling clinical findings in affected patients was observed in rats administered the two compounds.Crystal composition determination revealed the existence of melamine and uric acid in the affected kidneys,resembling human stones.Conclusion Our findings suggest that uric acid plays a key role in melamine-related kidney injury in humans.Future studies should consider uric acid together with melamine when examining adverse effects in humans. 展开更多
关键词 Melamine Nephrotoxicity Hyperuricemia Urolithiasis
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Nephrotoxicity and carcinogenesis of aristolochic acids and their derivates 认领 引用 被引量：1
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作者 Zi-Qi Jin Jin-Wei Yuan +1 位作者 Jian Hao Xiong-Zhi Wu 《Traditional Medicine Research》 2018年第1期1-9,共9页
Aristolochic acids （AAs）, a natural mixture of 8-methoxy-6-nitro-phenanthro-（3,4-d）-1,3-dioxolo-5-carboxylic acid （AAI）and 6-nitro-phenanthro-（3,4-d）-1,3-dioxolo-5-carboxylic acid （AAII）, derived from aristo... Aristolochic acids （AAs）, a natural mixture of 8-methoxy-6-nitro-phenanthro-（3,4-d）-1,3-dioxolo-5-carboxylic acid （AAI）and 6-nitro-phenanthro-（3,4-d）-1,3-dioxolo-5-carboxylic acid （AAII）, derived from aristolochiaceae species, has beenreported to cause AAS-induced nephropathy and upper urothelial cancer. In this review, we summarize the informationon the nephrotoxicity and carcinogenesis of AAs and their derivatives. AAs nephrotoxicity can lead to apoptosis andoxidative stress of renal tubular cells, and inhibition of the expression of aquaporins. AAs can also reduce the capabilityfor renal tubular epithelial cell repair after acute injury and further produce renal fibrosis by activating TGF-β-Smadsignaling and promoting the migration of macrophages. Moreover, AAs-induced carcinogenesis may be due to theformation of covalent adducts with DNA which can lead to the mutation in certain tumor suppressor genes orproto-oncogenes and the different catalyzing capacity of the microsomal cytochrome P450 of individuals in AAImetabolism. 展开更多
关键词 Aristolochic acids Aristolochic acids nephropathy Nephrotoxicity Carcinogenesis
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Probiotic bacteria attenuates cisplatin-induced nephrotoxicity through modulation of oxidative stress, inflammation and apoptosis in rats 认领 引用 被引量：2
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作者 Emin Sengul Sevda Ur?ar Gelen +2 位作者 Serkan Y?ld?r?m Fikret ?elebi Ali ??nar 《Asian Pacific Journal of Tropical Biomedicine》 SCIE CAS 2019年第3期116-122,共7页
Objective: To investigate the effects of probiotic bacteria on cisplatin(CP)-induced nephrotoxicity. Methods: In the present study, 50 Sprague-Dawley rats were used and randomly divided into five groups including cont... Objective: To investigate the effects of probiotic bacteria on cisplatin(CP)-induced nephrotoxicity. Methods: In the present study, 50 Sprague-Dawley rats were used and randomly divided into five groups including control, CP, probiotic bacteria treatment groups with different doses(0.5 and 1 mL) and only probiotic bacteria group. After CP and probiotic administration on seven days, rats sacrificed under anesthesia on the eighth day. The serum urea, creatinine, and blood urea nitrogen levels were analyzed. In renal tissue, malondialdehyde levels, superoxide dismutase and glutathione activity, interleukin-8, interleukin-1β and tumor necrosis factor-alpha levels were determined and histopathological and immunohistochemical changes were also examined. Results: According to results, urea, creatinine and blood urea nitrogen levels as well as kidney weights increased in CP group. Also, CP induced inflammation, oxidative stress, DNA damage and apoptosis in kidney tissue and caused histopathological changes. Administration of the high dose of probiotic bacteria could prevent these changes and damages. Conclusions: This study reveals that probiotic bacteria has protective effects on CP-induced renal damage in rats. 展开更多
关键词 Apoptosis Cisplatin Nephrotoxicity Probiotic Rat
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In vitro study of emodin-induced nephrotoxicity in human renal glomerular endothelial cells on a microfluidic chip 认领 引用
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作者 ZHUO YANG WEN QIN +5 位作者 DI CHEN JUNSHENG HUO JINGBO WANG LIYUAN WANG QIN ZHUO JIYONG YIN 《BIOCELL》 SCIE 2023年第1期125-131,共7页
Emodin is an effective component of rhubarb with positive pharmacological effects on human health.However,it is also toxic to different cells or tissues to varying degrees.The effects of emodin on glomerular endotheli... Emodin is an effective component of rhubarb with positive pharmacological effects on human health.However,it is also toxic to different cells or tissues to varying degrees.The effects of emodin on glomerular endothelial cells(GECs)remain to be tested,and the documented works were always performed in vitro and hardly reflect the real physiological situation.To study the effects of emodin on GECs in a biomimetic environment,we utilized a microfluidic chip to assess the physiological reaction of human renal glomerular endothelial cells to various concentrations of emodin in this work.The results showed that emodin caused cytotoxicity,impaired glomerular filtration barrier integrity to macromolecules,and increased barrier permeability in a dose-dependent manner.With the increase in emodin concentration,the concentration of the pro-inflammatory cytokine tumor necrosis factor-α,interleukin(IL)-6,transforming growth factor-β1,and monocyte chemoattractant protein(MCP-1)increased while the production of inflammatory cytokine IL-6 first increased and then decreased with the increase in emodin concentration.Our findings shed new light on emodin-induced nephrotoxicity and provide insights for the application of microfluidic chip devices to reveal drug-cell interactions. 展开更多
关键词 Emodin Nephrotoxicity HRGECs Microfluidic chip
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Dosage of L-arginine Preventing Acute High-dose PDD Nephrotoxicity 认领 引用
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作者 王京芬 刘秀菊 郝鲁英 《The Chinese-German Journal of Clinical Oncology》 2005年第6期358-360,共3页
Objective： To explore the optimal dose of L-arginine to prevent acute high-dose （HD）-PDD nephrotoxicity. Methods： 128 cases using PDD with the dosage of 100 mg/m^2 within two days （D1, 2） in combination with L-a... Objective： To explore the optimal dose of L-arginine to prevent acute high-dose （HD）-PDD nephrotoxicity. Methods： 128 cases using PDD with the dosage of 100 mg/m^2 within two days （D1, 2） in combination with L-arginine were randomly divided into 3 groups of A, B and C. The dosages of L- arginine in the 3 groups were 5 g/（m^2·d）, 10 g/（m^2·d） and 15 g/（m^2·d）, respectively. Each patient received 2 cycles chemotherapy to form self control： 1 cycle combined with L-arginine, while 1 cycle chemotherapy alone, β2-MG in urine, BUN, Cr and uric acid in blood were detected just 24 h before and after using PDD. The changes of each index in the three groups were observed in the presence or absence, and the therapeutic effects were compared among the three groups. Results： There was no significant difference in BUN, Cr and uric acid in blood before and after chemotherapy in the presence or absence, showing these indexes could not be used as markers of early acute nephrotoxicity. Urine β2-MG values in the presence and absence were 0.9120±0.6618 vs 1.5167±0.7908 （P〈0.05）, 0.5404±0.5810 vs 1.4616±0.8120 （P〈0.01）, 0.4998±0.6210 vs 1.5210±0.7710 （P〈0.01） in the groups A, B and C respectively. The excellent effective rate and total effective rate in groups A, B and C were 40.9% and 59.1%, 68.2% and 90.9%, and 77.5% and 97.5%, respectively. There was significant difference in the excellent effective rate and total effective rate between groups A and B, but not between groups B and C. Conclusion： The optimal dose of L- arginine to prevent acute HD-PDD nephrotoxicity is 10 g/（m^2·d）. Increased dosage can＇t improve the effect accordingly. 展开更多
关键词 L-arginine optimal dosage PDD nephrotoxicity
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Decursin Mediated Protection on Cisplatin-induced Nephrotoxicity in SD Rats and BDF1 Mice 认领 引用
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作者 Jiang Cheng-zhe Han Ilhyun Choung Seyoung 《Journal of Northeast Agricultural University(English Edition)》 CAS 2012年第1期50-56,共7页
Tisplatin is one of the valuable icancer agents against several types of neoplasm. However, nephrotoxicity is the major adverse effect representing in cisplatin therapy. In this study, the animal tests detecting prote... Tisplatin is one of the valuable icancer agents against several types of neoplasm. However, nephrotoxicity is the major adverse effect representing in cisplatin therapy. In this study, the animal tests detecting protective effects of a natural compound, Decursin, on cisplatin-induced nephrotoxicity were examined by using in vivo model. Pretreatment Decursin 10, 20 and 40 mg · kg^-1 at 48, 24 and 6 h, and administration of a single dose of Cisplatin 5.2 mg · kg^-1. Nephrotoxicity was evaluated by serum BUN and creatinine examination. There was significant difference in body weights, serum BUN and creatinine levels of the normal group. Based on the new understanding of the protective mechanisms of cisplatin-induced nephrotocivity, new strategies can be developed to prevent renal injury or to enhance recovery after cisplatin treatment. 展开更多
关键词 cisplatin Decursin nephrotoxicity rat mice
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In vitro study of the nephrotoxicity of total Dahuang(Radix Et Rhizoma Rhei Palmati) anthraquinones and emodin in monolayer human proximal tubular epithelial cells cultured in a transwell chamber 认领 引用 被引量：4
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作者 Cao Chunyu Hui Lianqiang +5 位作者 Li Chun Yang Yifei Zhang Jiyuan Liu Ting Hao Ran Zhang Yi 《Journal of Traditional Chinese Medicine》 SCIE CSCD 2019年第5期609-623,共15页
OBJECTIVE: To examine changes in the morphology and physiological functions of human proximal tubular epithelial cells (HK-2 cells) caused by total Dahuang (Radix Et Rhizoma Rhei Palmati) anthraquinones (TDA) and emod... OBJECTIVE: To examine changes in the morphology and physiological functions of human proximal tubular epithelial cells (HK-2 cells) caused by total Dahuang (Radix Et Rhizoma Rhei Palmati) anthraquinones (TDA) and emodin. METHODS: HK-2 cells were cultured on polycarbonate (PCF) membranes to form a complete monolayer of cells. A fluorescein isothiocyanate- dextran (FITC) permeability assay was conducted and secretion of γ-glutamyltranspeptidase (GGT), lactate dehydrogenase (LDH), N-acetyl-β-D-glucosaminidase (NAG) and kidney injury molecule 1 (KIM-1) was examined. The reabsorption of glucose and the excretion of para-aminohippuric acid (PAH) by HK-2 cells were also examined. The morphology of HK-2 cells was observed using optical microscopy and scanning electron microscopy. The cytoskeleton of HK-2 cells was observed under a fluorescence microscope. RESULTS: Compared with the results for the dimethyl sulfoxide group, treatment of cells with TDA and emodin showed statistically significant differences in the FITC leakage rate, the apical / basolateral ratio of LDH and GGT, and the secretion of GGT, LDH, NAG and KIM-1. At 64 μg/mL, TDA markedly inhibited blood glucose reabsorption and remarkably suppressed PAH excretion by HK-2 cells. Both TDA and emodin caused various degrees of damage to the morphology and cytoskeleton of HK-2 cells with the degree of damage correlating positively with the dosage of the tested substances.CONCLUSION: Both TDA and emodin caused damage to human renal proximal tubular epithelial cells at certain dosages. At the same dosage, TDA caused more severe damage than emodin to the HK-2 cells. 展开更多
关键词 Anthraquinones Rheum Emodin Nephrotoxicity Human proximal tubular epithelial cell Transwell chamber
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Effect of Helichrysum plicatum DC. subsp. plicatum ethanol extract on gentamicin-induced nephrotoxicity in rats 认领 引用 被引量：5
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作者 Betul APAYDIN YILDIRIM Saban KORDALI +3 位作者 Kubra Asena TERIM KAPAKIN Fatih YILDIRIM Esra AKTAS SENOCAK Serdar ALTUN 《Journal of Zhejiang University-SCIENCE B》 SCIE CAS CSCD 2017年第6期501-511,共11页
The aim of this study was to evaluate the possible therapeutic or protective effects of Helichrysum plicatum DC.subsp.plicatum ethanol extract（HPE）against gentamicin-induced nephrotoxicity.Thirty-six Sprague Dawley ... The aim of this study was to evaluate the possible therapeutic or protective effects of Helichrysum plicatum DC.subsp.plicatum ethanol extract（HPE）against gentamicin-induced nephrotoxicity.Thirty-six Sprague Dawley male rats weighing between 200 and 250 g were used as live material.They were formed into six groups containing 6rats each and were allowed to adapt to laboratory conditions for 7 d.Group Ⅰ：control,5%DMSO intraperitoneal（i.p.）;Group Ⅱ：HPE 100 mg/（kg·d）i.p.;Group Ⅲ：HPE 200 mg/（kg·d）i.p.;Group Ⅳ：gentamicin as 80 mg/（kg·d）i.p.;Group Ⅴ：gentamicin as 80 mg/（kg·d）i.p.＋HPE 100 mg/（kg·d）i.p.;and Group Ⅵ：gentamicin as 80 mg/（kg·d）i.p.＋HPE 200 mg/（kg·d）i.p.for 8 d.Following treatment,serum,liver,and kidney tissues were used to assess blood urea nitrogen（BUN）,creatinine,enzymatic and non-enzymatic antioxidants,and lipid peroxidation.Gentamicin significantly increased serum BUN,creatinin,and liver and kidney levels of malondialdehyde（MDA）.It also decreased the activity of catalase（CAT）,glutathione peroxidase（GPx）,and superoxide dismutase（SOD）.Treatment with the HPE 100 mg/kg reversed gentamicin-induced alterations as evidenced by decreased serum BUN and creatinin,liver and kidney oxidant marker,and tubular necrosis as well as by an increase in antioxidant enzymes.It was found that HPE 200 mg/kg significantly increased liver and kidney tissue MDA levels in nephrotoxicity in rats.As a result,these findings support the proposition that HPE in 100 mg/kg dose demonstrates in the kidney and liver as free radicals and scavenger to prevent the toxic effects of gentamicin in both the biochemical and histopathology parameters. 展开更多
关键词 Antioxidants Extract Gentamicin Helichrysum plicatum DC. subsp. plicatum Nephrotoxicity Oxidative stress
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Liposomes for systematic delivery of vancomycin hydrochloride to decrease nephrotoxicity:Characterization and evaluation 认领 引用 被引量：5
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作者 Junli Liu Zhonglan Wang +3 位作者 Fubing Li Jinhua Gao Longmei Wang Guihua Huang 《Asian Journal of Pharmaceutical Sciences》 SCIE CAS 2015年第3期212-222,共11页
Vancomycin hydrochloride(VANH),the first glycopeptide antibiotic,is a water-soluble drug for the treatment of acute osteomyelitis.Liposomal formulations of VANH have already been manipulated and characterized,which wa... Vancomycin hydrochloride(VANH),the first glycopeptide antibiotic,is a water-soluble drug for the treatment of acute osteomyelitis.Liposomal formulations of VANH have already been manipulated and characterized,which was a mean of increasing their therapeutic index,reducing their toxicity and altering drug biodistribution.One of the challenges for preparing VANH-Lips is their low encapsulation efficiency(EE).In the present study,we aim to improve the liposomal formulation of VANH for higher EE,longer systemic circulation,reduced nephrotoxicity and enhanced antimicrobial activities.Vancomycin hydrochloride-loaded liposomes(VANH-Lips)were formulated by the method of modified reverse phase evaporation.Based on the optimization of formulation with orthogonal experimental design,the average drug encapsulation efficiency and the mean particle size of VANH-Lips were found to be 40.78±2.56%and 188.4±2.77 nm.In vitro drug release of VANH-Lips possessed a sustained release characteristic and their release behavior was in accordance with the Weibull equation.After intravenous injection to mice,the mean residence time(MRT)of VANH-Lips group was significantly prolonged in vivo and the AUC value was improved as well compared with the vancomycin hydrochloride solution(VANH-Sol)group.Furthermore,the biodistribution results in mice showed that VANH-Lips decreased the accumulation of VANH in kidney after intravenous injection.In conclusion,VANH-Lips may be a potential delivery system for VANH to decrease nephrotoxicity in the treatment of osteomyelitis. 展开更多
关键词 Biodistribution Nephrotoxicity Pharmacokinetic Systematic delivery Vancomycin hydrochloride liposome
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Toxicity Evaluation of Freshwater Cyanobacterium Microcystis aeruginosa PCC 7806: Ⅱ Nephrotoxicity in Rats 认领 引用 被引量：8
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作者 R. BHATTACHARYA K. SUGENDRAN +1 位作者 R. S. DANGI AND P. V. LAKSHMANA RAO (Address correspondence t 《Biomedical and Environmental Sciences》 SCIE CAS 1997年第1期93-101,共9页
Nephrotoxic potential of laboratory cultures of freshwater cyanobacterium (blue-green al ga) Microcystis aeruginosa PCC 7806 (Pasteur Institute) was assessed in male rats. The ani mals were injected intraperitoneally ... Nephrotoxic potential of laboratory cultures of freshwater cyanobacterium (blue-green al ga) Microcystis aeruginosa PCC 7806 (Pasteur Institute) was assessed in male rats. The ani mals were injected intraperitoneally with 0. 5, 1. 0 and 2. 0 LD50 doses of lyophilized cell ex tract. Elevated plasma urea and creatinine levels were accompanied by decrease in protein and albumin levels, followed by hematuria, proteinuria and bilirubinuria. Also decrease in kidney lactate dehydrogenase and glutamic oxaloacetic transaminase indicated possible nephrotoxic po tential of the cyanobacteria. The extract also produced various hematological changes associat ed with stagnant type of hypoxia. High perfomance liquid chromatography of the culture I dentified the active principle (toxin) as Microcystin-LR 展开更多
关键词 PCC Nephrotoxicity in Rats Toxicity Evaluation of Freshwater Cyanobacterium Microcystis aeruginosa PCC 7806
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