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Schisandra chinensis Oil Attenuates Aristolochic Acid Ⅰ-Induced Nephrotoxicity in vivo and in vitro

Chinese Journal of Integrative Medicine 2022年第7期28卷 603-611页

作者： YANG Yan GE Fei-lin ZHAN Xiao-yan MU Wen-qing LI Zhi-yong LIN Li WEI Zi-ying BAI Zhao-fang SUN Qin XIAO Xiao-he School of Integrated Traditional Chinese and Western Medicine Southwest Medical UniversityLuzhouSichuan Province 646000China Senior Department of Hepatology the Fifth Medical Center of PLA General HospitalBeijing 100039China China Military Institute of Chinese Materia the Fifth Medical Center of PLA General HospitalBeijing 100039China

Objective: To investigate the protective effects of Schisandra chinensis oil(SCEO) against aristolochic acid Ⅰ(AAⅠ)-induced Nephrotoxicity in vivo and in vitro and elucidate the underlying mechanism.Methods: C57BL/6 mice were randomly divided into 5 groups according to a random number table, including control group, AAⅠ group, and AAⅠ+SCEO(0.25, 0.5 and 1 g/kg) groups(n=5 per group). Pretreatment with SCEO was done for 2 days by oral administration, while the control and AAⅠ groups were treated with sodium carboxymethyl cellulose. Mice of all groups except for the control group were injected intraperitoneally with AAⅠ(5 mg/kg) from day 3 until day 7. Histopathological examination and apoptosis of kidney tissue were observed by hematoxylin and eosin and TdT-mediated dUTP nick-end labeling(TUNEL) staining, respectively. The levels of serum alanine aminotransferase(ALT), aspartate aminotransferase(AST), blood urea nitrogen(BUN), and serum creatinine(SCr), as well as renal malondialdehyde(MDA), glutathione, r-glutamyl cysteingl+glycine(GSH), and superoxide dismutase(SOD) were analyzed using enzyme-linked immunosorbent assay(ELISA).Expressions of hepatic cytochrome P450 1A1(CYP1A1), CYP1A2, and nad(p)hquinonedehydrogenase1(NQO1) were analyzed using ELISA, quantitative real-time polymerase chain reaction(qPCR) and Western blot,respectively. In vitro, SCEO(40 μg/mL) was added 12 h before treatment with AAⅠ(40 μmol/mL for 48 h) in human renal proximal tubule cell line(HK-2), then apoptosis and reactive oxygen species(ROS) were analyzed by flow cytometry. Results: SCEO 0.5 and 1 g/kg ameliorated histopathological changes and TUNEL+ staining in the kidney tissues of mice with AAⅠ-induced Nephrotoxicity, and reduced serum levels of ALT, AST, BUN and SCr(P<0.01 or P<0.05). SCEO 0.5 and 1 g/kg alleviated the ROS generation in kidney, containing MDA,GSH and SOD(P<0.01 or P<0.05). SCEO 1 g/kg increased the expressions of CYP1A1 and CYP1A2 and decreased NQO1 level in the liver tissues(P<0.01 or P<0.05). Besides, in vitro studies

关键词： aristolochic acidⅠ Nephrotoxicity Schisandra chinensis oil metabolic enzymes apoptosis reactive oxygen species

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In vitro study of emodin-induced Nephrotoxicity in human renal glomerular endothelial cells on a microfluidic chip

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BIOCELL 2023年第1期47卷 125-131页

作者： ZHUO YANG WEN QIN DI CHEN JUNSHENG HUO JINGBO WANG LIYUAN WANG QIN ZHUO JIYONG YIN National Institute for Nutrition and Health Chinese Center for Disease Control and PreventionBeijing100050China

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.

关键词： Emodin Nephrotoxicity HRGECs Microfluidic chip

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Melatonin alleviates oxidative stress,inflammation,apoptosis,and DNA damage in acrylamide-induced Nephrotoxicity in rats

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Asian Pacific Journal of Tropical Biomedicine 2023年第3期13卷 121-130页

作者： Fatmaİbaokurgil Hakan Aydin Serkan Yildirim Emin Sengul Department of Physiology Faculty of Veterinary MedicineAtatürk UniversityErzurumTurkey Department of Virology Faculty of Veterinary MedicineAtatürk UniversityErzurumTurkey Department of Pathology Faculty of Veterinary MedicineAtatürk UniversityErzurumTurkey

Objective:To investigate the effects of melatonin on renal inflammation,oxidative stress,apoptosis,as well as DNA and tissue damage in acrylamide-induced Nephrotoxicity in rats.Methods:Fifty male rats were randomly divided into five groups.The control group received distilled water by gastric lavage for 11days and the acrylamide group was administered acrylamide(50 mg/kg,i.g.)for 11 days.The MEL10+ACR and MEL20+ACR groups received intraperitoneal melatonin 10 and 20 mg/kg,respectively,for 11 days,and acrylamide(50 mg/kg,i.g.)was administered 1h after melatonin injection.The MEL20 group was injected with melatonin(20 mg/kg)for 11 days.Kidney function tests were performed and biochemical and inflammatory parameters were determined.In addition,histopathological,immunohistochemical,and immunofluorescence examinations were carried out.Results:Melatonin significantly abated acrylamide-induced rise in serum urea and creatinine levels.Acrylamide caused oxidative stress,inflammation,apoptosis,as well as DNA and tissue damage in the kidneys.Melatonin treatment alleviated acrylamide-induced renal damage by exhibiting antioxidant,anti-inflammatory,and antiapoptotic effects.Moreover,melatonin significantly ameliorated acrylamide-caused histopathological changes in kidney tissue.Conclusions:Melatonin attenuates acrylamide-induced renal oxidative stress,inflammation,apoptosis,and DNA damage in rats.

关键词： Acrylamide Apoptosis Inflammation Melatonin Nephrotoxicity Oxidative stress Rat

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Altered cisplatin pharmacokinetics during nonalcoholic steatohepatitis contributes to reduced Nephrotoxicity

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Acta Pharmaceutica Sinica B 2021年第12期11卷 3869-3878页

作者： Joseph L.Jilek Kayla L.Frost Kevyn A.Jacobus Wenxi He Erica L.Toth Michael Goedken Nathan J.Cherrington Department of Pharmacology&Toxicology College of PharmacyUniversity of ArizonaTucsonAZ 85724USA Rutgers Translational Sciences Rutgers UniversityPiscatawayNJ 08901USA

Disease-mediated alterations to drug disposition constitute a significant source of adverse drug reactions.Cisplatin(CDDP)elicits Nephrotoxicity due to exposure in proximal tubule cells during renal secretion.Alterations to renal drug transporter expression have been discovered during nonalcoholic steatohepatitis(NASH),however,associated changes to substrate toxicity is unknown.To test this,a methionine-and choline-deficient diet-induced rat model was used to evaluate NASH-associated changes to CDDP pharmacokinetics,transporter expression,and toxicity.NASH rats administered CDDP(6 mg/kg,i.p.)displayed 20%less Nephrotoxicity than healthy rats.Likewise,CDDP renal clearance decreased in NASH rats from 7.39 to 3.83 mL/min,renal secretion decreased from 6.23 to 2.80 mL/min,and renal CDDP accumulation decreased by 15%,relative to healthy rats.Renal copper transporter-1 expression decreased,and organic cation transporter-2 and ATPase copper transporting protein-7 b increased slightly,reducing CDDP secretion.Hepatic CDDP accumulation increased 250%in NASH rats relative to healthy rats.Hepatic organic cation transporter-1 induction and multidrug and toxin extrusion protein-1 and multidrug resistance-associated protein-4 reduction may contribute to hepatic CDDP sequestration in NASH rats,although no drug-related toxicity was observed.These data provide a link between NASH-induced hepatic and renal transporter expression changes and CDDP renal clearance,which may alter Nephrotoxicity.

关键词： Nonalcoholic steatohepatitis NASH Cisplatin Drug transporter Nephrotoxicity

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Organic anion transporter 1 and 3 contribute to traditional Chinese medicine-induced Nephrotoxicity

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Chinese Journal of Natural Medicines 2020年第3期18卷 196-205页

作者： SHEN Qing-Qing WANG Jing-Jing ROY Debmalya SUN Li-Xin JIANG Zhen-Zhou ZHANG Lu-Yong HUANG Xin Jiangsu Key Laboratory of Drug Screening China Pharmaceutical UniversityNanjing 210009China Jiangsu Center for Pharmacodynamics Research and Evaluation China Pharmaceutical UniversityNanjing 210009China Key Laboratory of Drug Quality Control and Pharmacovigilance Ministry of EducationChina Pharmaceutical UniversityNanjing 210009China Center for Drug Screening and Pharmacodynamics Evaluation School of PharmacyGuangdong Pharmaceutical UniversityGuangzhou 510006China

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.

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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Protective effect of Cistanche deserticola on gentamicin-induced Nephrotoxicity in rats

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Chinese Herbal Medicines 2023年第1期15卷 102-109页

作者： Xiaoqing Song Jinying Wang Yu Zhang Xinqian Du Qibing Qian Basic Medical College of Hebei North University Zhangjiakou 075000China

Objective: Gentamicin(GM) is a commonly used aminoglycoside antibiotic, however, renal toxicity has limited its usage. The present study was designed to evaluate the ameliorative effect of Cistanche deserticola on GM-induced Nephrotoxicity in rats.Methods: The Nephrotoxicity in rats was induced by intraperitoneal administration of GM(100 mg/kg)for 10 consecutive days. Glomerular filtration rate, blood urea nitrogen, creatinine and kidney histopathology were detected to assess the GM-induced Nephrotoxicity. The oxidative stress(catalase,superoxide dismutase, glutathione and malondialdehyde) was assessed. The inflammatory response(tumor necrosis factor-a, interleukin-6, myeloperoxidase and nuclear factor-kappa B) and apoptotic marker(Bax and Bcl-2) were also evaluated.Results: The results showed that water and 75% ethanol extracts of C. deserticola(named CDW and CDE,respectively)(100, 200 and 400 mg/kg) in combination with GM could recover the reduction of glomerular filtration rate and enhance the renal endogenous antioxidant capability induced by GM. The increase in the expression of renal inflammatory cytokines(tumor necrosis factor-a and interleukin-6), nuclear protein of nuclear factor-kappa B(p65) and the activity of myeloperoxidase induced by GM was significantly decreased upon CDW or CDE treatment. In addition, CDW or CDE treatment could decrease the Bax protein expression and increase the Bcl-2 protein expression in GM-induced Nephrotoxicity in rats significantly.Conclusion: The study demonstrated that C. deserticola treatment could attenuate kidney dysfunction and structural damage in rats induced by GM through the reduction of inflammation, oxidative stress and apoptosis.

关键词： apoptosis Cistanche deserticola Y.C.Ma gentamicin inflammation Nephrotoxicity Orobanchaceae oxidative stress

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In situ metabolomics in Nephrotoxicity of aristolochic acids based on air flow-assisted desorption electrospray ionization mass spectrometry imaging

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Acta Pharmaceutica Sinica B 2020年第6期10卷 1083-1093页

作者： Zhonghua Wang Bingshu He Yaqi Liu Meiling Huo Wenqing Fu Chunyan Yang Jinfeng Wei Zeper Abliz Center for Imaging and Systems Biology College of Life and Environmental SciencesMinzu University of ChinaBeijing 100081China New Drug Safety Evaluation Center Institute of Materia MedicaPeking Union Medical CollegeBeijing 100050China Key Laboratory of Ethnomedicine of Ministry of Education Minzu University of ChinaBeijing 100081China School of Pharmacy Minzu University of ChinaBeijing 100081China

Understanding of the Nephrotoxicity induced by drug candidates is vital to drug discovery and development.Herein,an in situ metabolomics method based on air flow-assisted desorption electrospray ionization mass spectrometry imaging(AFADESI-MSI)was established for direct analysis of metabolites in renal tissue sections.This method was subsequently applied to investigate spatially resolved metabolic profile changes in rat kidney after the administration of aristolochic acid I,a known nephrotoxic drug,aimed to discover metabolites associated with Nephrotoxicity.As a result,38 metabolites related to the arginine-creatinine metabolic pathway,the urea cycle,the serine synthesis pathway,metabolism of lipids,choline,histamine,lysine,and adenosine triphosphate were significantly changed in the group treated with aristolochic acid I.These metabolites exhibited a unique distribution in rat kidney and a good spatial match with histopathological renal lesions.This study provides new insights into the mechanisms underlying aristolochic acids Nephrotoxicity and demonstrates that AFADESI-MSI-based in situ metabolomics is a promising technique for investigation of the molecular mechanism of drug toxicity.

关键词： Aristolochic acid Nephrotoxicity Mass spectrometry imaging In situ metabolomics AFADESI

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Chinese Medicine Might Be A Promising Way for A Solution to Arsenic Nephrotoxicity

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Chinese Journal of Integrative Medicine 2020年第2期26卷 83-87页

作者： GONG Xue-zhong Department of Nephrology Shanghai Municipal Hospital of Traditional Chinese Medicine Shanghai University of Traditional Chinese Medicine

Arsenic from environmental contamination is a risk factor for kidney disease,and the clinical use of arsenic also triggers a new concern that the potential kidney damage caused by exposure to clinical doses of arse nic trivale nt.So far,the un dergoi ng mecha nisms con tributi ng to arse nic n ephrotoxicity mostly remain unclear,and universally accepted methods for preventing this complication are limited too.Ancient Chinese medical scientists recognized the toxicity of arsenic long ago,and there were some records of Chinese herbs against arsenic poisoning in ancient books of Chinese medicine.In the past decade,several herbal formulations,as well as some potentially active compounds extracted from Chinese herbs,have been employed to prevent arsenic Nephrotoxicity both in vivo and in vitro and showed better therapeutic effects.The present paper thus summarizes and discusses these Chinese medicine methods in preventing such a public health problem.In addition,we call for large,well-desig ned,randomized,and controlled clinical trials to be performed to further assess the efficacy and safety of these potential methods of Chinese medicine against arsenic Nephrotoxicity.

关键词： arsenic Nephrotoxicity Chinese medicine therapy acute kidney injury

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Cilastatin protects against imipenem-induced Nephrotoxicity via inhibition of renal organic anion transporters(OATs)

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Acta Pharmaceutica Sinica B 2019年第5期9卷 986-996页

作者： Xiaokui Huo Qiang Meng Changyuan Wang Yanna Zhu Zhihao Liu Xiaodong Ma Xiaochi Ma Jinyong Peng Huijun Sun Kexin Liu Department of Clinical Pharmacology College of PharmacyDalian Medical UniversityDalian116044China College(Institute)of Integrative Medicine Dalian Medical UniversityDalian116044China Provincial Key Laboratory for Pharmacokinetics and Transport Dalian Medical UniversityDalian116044China

Imipenem is a carbapenem antibiotic. However, Imipenem could not be marketed owing to its instability and Nephrotoxicity until cilastatin, an inhibitor of renal dehydropeptidase-I(DHP-I),was developed. In present study, the potential roles of renal organic anion transporters(OATs) in alleviating the Nephrotoxicity of imipenem by cilastatin were investigated in vitro and in rabbits. Our results indicated that imipenem and cilastatin were substrates of h OAT1 and h OAT3. Cilastatin inhibited h OAT1/3-mediated transport of imipenem with IC50 values comparable to the clinical concentration, suggesting the potential to cause a clinical drug–drug interaction(DDI). Moreover,imipenem exhibited h OAT1/3-dependent cytotoxicity, which was alleviated by cilastatin and probenecid. Furthermore, cilastatin and probenecid ameliorated imipenem-induced rabbit acute kidney injury, and reduced the renal secretion of imipenem. Cilastatin and probenecid inhibited intracellular accumulation of imipenem and sequentially decreased the nephrocyte toxicity in rabbit primary proximal tubule cells. Renal OATs, besides DHP-I, was also the target of interaction between imipenem and cilastatin, and contributed to the Nephrotoxicity of imipenem. This therefore gives in part the explanation about the mechanism by which cilastatin protected against imipenem-induced Nephrotoxicity. Thus, OATs can potentially be used as a therapeutic target to avoid the renal adverse reaction of imipenem in clinic.

关键词： Imipenem Cilastatin Probenecid OATs h OAT1 h OAT3 Nephrotoxicity

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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

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Journal of Traditional Chinese Medicine 2019年第5期39卷 609-623页

作者： Cao Chunyu Hui Lianqiang Li Chun Yang Yifei Zhang Jiyuan Liu Ting Hao Ran Zhang Yi Safety Evaluation Center for Chinese Materia Medica Institute of Chinese Materia MedicaChina Academy of Chinese Medical SciencesBeijing 100700China Quality Standard Center for Chinese Materia Medica Institute of Chinese Materia MedicaChina Academy of Chinese Medical SciencesBeijing 100700China Department of Sciences and Education Institute of Chinese Materia MedicaChina Academy of Chinese Medical SciencesBeijing 100700China Pharmacology Research Center for Chinese Materia Medica Institute of Chinese Materia MedicaChina Academy of Chinese Medical SciencesBeijing 100700China

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.

关键词： Anthraquinones Rheum Emodin Nephrotoxicity Human proximal tubular epithelial cell Transwell chamber

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