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Urinary cystatin C:pediatric reference intervals and comparative assessment as a biomarker of renal injury among children in the regions with high burden of CKDu in Sri Lanka

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World Journal of Pediatrics 2022年第3期18卷 196-205页

作者： Patabandi Maddumage Mihiri Ayesha Sandamini Pallage Mangala Chathura Surendra De Silva Thibbotuwa Deniya Kankanamge Sameera Chathuranga Gunasekara Sakuntha Dewaka Gunarathna Ranawake Arachchige Isini Pinipa Chula Herath Sudheera Sammanthi Jayasinghe Ediriweera Patabandi Saman Chandana Nishad Jayasundara Department of Zoology Faculty of ScienceUniversity of RuhunaMatara 81000Sri Lanka Department of Nephrology Sri Jayewardenepura General HospitalColombo 10100Sri Lanka Department of Pharmacology Faculty of MedicineUniversity of RuhunaGalle 80000Sri Lanka Department of Biosystems Technology Faculty of TechnologyUniversity of RuhunaMatara 81000Sri Lanka The Nicholas School of the Environment Duke UniversityDurhamNC 27708USA

Background Cystatin C(Cys-C)is an emerging biomarker of renal diseases and its clinical use,particularly for screening the communities affected by chronic kidney disease of unknown etiology(CKDu),is hindered due to the lack of reference intervals(RIs)for diverse ethnic and age groups.The present study aimed to define RIs for urinary Cys-C(uCys-C)for a healthy pediatric population in Sri Lanka and in turn compare the renal function of the residential children in CKDu endemic and non-endemic regions in Sri Lanka.Methods A cross-sectional study was conducted with 850 healthy children(10-17 years)from selected locations for reference interval establishment,while a total of 892 children were recruited for the comparative study.Urine samples were collected and analyzed for Cys-C,creatinine(Cr)and albumin.Cr-adjusted uCys-C levels were partitioned by age,and RIs were determined with quantile regression(2.5th,50th and 97.5th quantiles)at 90%confidence interval.Results The range of median RIs for uCys-C in healthy children was 45.94-64.44 ng/mg Cr for boys and 53.58-69.97 ng/mg Cr for girls.The median(interquartile range)uCys-C levels of children in the CKDu endemic and non-endemic regions were 58.18(21.8-141.9)and 58.31(23.9-155.3)ng/mg Cr with no significant difference(P=0.781).A significant variation of uCys-C was noted in the children across age.Conclusions Notably high uCys-C levels were observed in children with elevated proteinuria.Thus,uCys-C could be a potential biomarker in identifying communities at high risk of CKDu susceptibility.

关键词： Chronic kidney disease of unknown etiology Cystatin C Pediatric Reference intervals renal injury Urinary albumin-creatinine ratio

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Salvianolic acid A alleviates renal injury in systemic lupus erythematosus induced by pristane in BALB/c mice

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Acta Pharmaceutica Sinica B 2017年第2期7卷 159-166页

作者： Yihuang Lin Yu Yan Huifang Zhang Yucai Chen Yangyang He Shoubao Wang Lianhua Fang Yang Lv Guanhua Du State Key Laboratory of Bioactive Substances and Functions of Natural Medicines Institute of Materia MedicaChinese Academy of Medical Sciences and Peking Union Medical College State Key Laboratory of Cardiovascular Disease Fuwai HospitalNational Center for Cardiovascular Diseases Beijing Key Laboratory of Drug Targets Identification and Drug Screening Institute of Materia MedicaChinese Academy of Medical Sciences and Peking Union Medical College Beijing Key Laboratory of Polymorphic Drugs Institute of Materia MedicaChinese Academy of Medical Sciences and Peking Union Medical College

The purpose of this study was to investigate the effects of salvianolic acid A(SAA) in systemic lupus erythematosus(SLE) induced by pristane in BALB/c mice.Lupus mice were established by confirming elevated levels of autoantibodies and IL-6 after intraperitoneal injection of pristane.Mice were then treated with daily oral doses of SAA for 5 months in parallel with mice treated with prednisone and aspirin as positive controls.The levels of autoantibodies were monitored at monthly intervals and nephritic symptoms observed by hematoxylin and eosin(H&E) and periodic acid-Schiff(PAS) staining.Western blot analysis of renal tissue was also employed.SAA treatment caused a significant reduction in the levels of anti-Sm autoantibodies and reduced renal histopathological changes and pathological effects.SAA treatment also significantly inhibited the phosphorylation of IKK,IκB and NFκB in renal tissues of lupus mice.In conclusion,the results suggest that SAA alleviates renal injury in pristane-induced SLE in BALB/c mice through inhibition of phosphorylation of IKK,IκB and NFκB.

关键词： Salvianolic acid A SLE renal injury Autoantibodies Pristane BALB/c mice NFκB

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Vitamin C Attenuates Hemorrhagic Shock-induced Dendritic Cell-specific Intercellular Adhesion Molecule 3-grabbing Nonintegrin Expression in Tubular Epithelial Cells and renal injury in Rats

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Chinese Medical Journal 2016年第14期129卷 1731-1736页

作者： Li Ma Jian Fei Ying Chen Bing Zhao Zhi-Tao Yang Lu Wang Hui-Qiu Sheng Er-Zhen Chen En-Qiang Mao Department of Emergency Medicine Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine Shanghai 200025 China Department of General Surgery Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine Shanghai 200025 China

Background： The expression of dendritic cell-specific intercellular adhesion molecule 3-grabbing nonintegrin （DC-SIGN） in renal tubular epithelial cells has been thought to be highly correlated with the occurrence of several kidney diseases, but whether it takes place in renal tissues during hemorrhagic shock （HS） is unknown. The present study airned to investigate this phenomenon and the inhibitory effect of Vitamin C （VitC）. Methods： A Sprague Dawley rat HS model was established in vivo in this study. The expression level and location of DC-SIGN were observed in kidneys. Also, the degree of histological damage, the concentrations of tumor necrosis factor-or and interleukin-6 in the renal tissues, and the serum concentration of blood urea nitrogen and creatinine at different times （2-24 h） alter HS （six rats in each group）, with or without VitC treatment belbre resuscitation, were evaluated. Results： HS induced DC-SIGN expression in rat tubular epithelial cells. The proinflarnmatory cytokine concentration, histological damage scores, and functional injury of kidneys had increased. All these phenornena induced by HS were relieved when the rats were treated with VitC before resuscitation. Conclusions： The results of the present study illustrated that HS could induce tubular epithelial cells expressing DC-SIGN, and the levels of proinflarnmatory cytokines in the kidney tissues improved correspondingly. The results also indicated that VitC could suppress the DC-SIGN expression in the tubular epithelial cells induced by HS and alleviate the inflammation and functional injury in the kidney.

关键词： Dendritic Cell-specific Intercellular Adhesion Molecule 3-grabbing Nonintegrin Hemorrhagic Shock renal injury Tubular Epithelial Cells Vitamin C

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Role of Reactive Oxygen Species in Triptolide-induced Apoptosis of renal Tubular Cells and renal injury in Rats

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Journal of Huazhong University of Science and Technology(Medical Sciences) 2011年第3期31卷 335-341页

作者：杨帆卓荦 Sunnassee Ananda 孙婷怡李上勋刘良 Faculty of Forensic Medicine Tongji Medical CollegeHuazhong University of Science and Technology

This study investigated the role of reactive oxygen species（ROS） in the pathogenesis of triptolide-induced renal injury in vivo.Rats were randomly divided into 4 groups（n=5 in each）：triptolide group in which the rats were intraperitoneally injected with triptolide solution at a dose of 1 mg/kg of body weight on day 8;control group in which the rats received a single intraperitoneal injection of 0.9% physiological saline on day 8;vitamin C group in which the rats were pretreated with vitamin C by gavage at a dose of 250 mg/kg of body weight per day for 7 days before the same treatment as the control group on day 8;triptolide＋vitamin C group in which the rats were first subjected to an oral administration of vitamin C at a dose of 250 mg/kg of body weight per day for 7 days,and then to the same treatment as the triptolide group on day 8.All the rats were sacrificed on day 10.Blood samples were collected for detection of plasma creatinine（Pcr） and plasma urea nitrogen（PUN） concentrations.Both kidneys were removed.The histological changes were measured by haematoxylin-eosin（HE） staining.The production of ROS was determined by detecting the fluorescent intensity of the oxida-tion-sensitive probe rhodamine 123 in renal tissue.renal malondialdehyde（MDA） content was meas-ured to evaluate lipid peroxidation level in renal tissue.TUNEL staining was performed to assess apop-tosis of renal tubular cells.renal expression of apoptosis-related proteins Bcl-2,Bax,Bid,Bad,Fas and FasL,as well as corresponding encoding genes were assessed by Western Blotting and real-time PCR.The results showed that triptolide treatment promoted the generation of a great amount of ROS,up-regulated the expression of Bax,Bid,Bad,Fas and FasL at both protein and mRNA levels,as well as the ratio of Bax to Bcl-2,and caused the apoptosis of renal tubular cells and renal injury.However,pretreatment with an antioxidant,vitamin C,significantly reduced the generation of ROS and effectively inhibited the triptolide-induced apoptosis of renal tubular cells an

关键词： triptolide reactive oxygen species apoptosis renal injury

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CD38 deficiency activates ERK1/2-NF-κB signaling pathway in sepsis-associated renal injury

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实验与检验医学 2022年第1期40卷 129-138页

作者： ZHANG Huiqing DU Yuna XIE Zhengyu WANG Zeyu LI Hua 李蓉 Department of Clinical Laboratory Jiangxi Provincial People's Hospital&The first Affiliated Hospital of Nanchang Medical CollegeNanchangChina Department of Clinical Laboratory the Second Affiliated Hospital of Nanchang University&Jiangxi Provincial Key Laboratory for Laboratory MedicineNanchangChina

CD38 is known to play roles in various inflammatory pathways.However,whether it has a protective or detrimental effect during bacterial septicemia remains disputed.Herein,this study aimed to determine the potential effect of CD38 on renal injury in septicemia.Escherichia coli(E.coli)was used to induce sepsis-associated renal injury in mice.WT and CD38-/-mice were stimulated with E.coli.After three hours,the serum was collected to detect renal function.Function mRNA expressions inflammatory cytokines in kidneys were quantified by real-time PCR.Hematoxylin and eosin staining were used to observe the histomorphology of kidney.The expression of TLR4,NF-κB,MAPK and cytokines were detected by Western Blot.Our results demonstrated that 3×10^(8) cfu/mL E.coli is the appropriate dose to induce sepsis mice model.Compared to WT sepsis mice,CD38-/-mice showed aggravated kidney injuries with impaired renal function,increased inflammation and apoptosis after E.coli stimulation.Interestingly,CD38 deficiency also led to elevated expression of TLR4 and increased phosphorylation of NF-κB p65/p105 and ERK1/2.To sum up,our results suggested that CD38 deficiency could aggravate E.coli-induced renal injury through activating ERK1/2-NF-κB signaling pathway.

关键词： CD38 ERK1/2 NF-κB sepsis renal injury

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The p53-mediated Apoptosis in Hypercholesterolemia-induced renal injury of Rats

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Journal of Huazhong University of Science and Technology(Medical Sciences) 2005年第4期25卷 408-411页

作者：姚颖田兴奎刘晓城邵菊芳吕永曼 Department of Nephrology Tongji Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan 430030 China

Summary： The apoptosis and the expression of tumor suppressor gene p53 in hypercholesterolemia （HC）-induced renal injury were investigated in rats. A high cholesterol diet （HCD）-induced HC rat model was made and serum lipid, urinary protein excretion （UPE） and N-aceto-β-D-glucosidase （NAG） were measured. The levels of malondialdehyde （MDA）, as an index of lipid peroxidation, in renal cortex and serum were compared between the two diet groups. Apoptosis and p53 expression were determined by TUNEL and immunohistochemistry, respectively. In the HCD-induced HC group, serum total cholesterol （TC）, low density lipoprotein cholesterol （LDL-C） as well as triglyceride （TG） were significantly increased, while the level of high density lipoprotein cholesterol （HDL-C） decreased. Meanwhile, increased excretions of UPE and NAG in urine were observed, which were accompanied with a decrease in urinary creatinine clearance （Ccr） and indicated both glomerular and tubular damages. In addition, apoptotic cell death coexisted in the kidney, as revealed by increased TUNEL positive cells. Finally, an increase in p53 expression was observed in tubuli, but not in glomeruli. Both TUNEL positive cells and p53 expression were found to be correlated to the level of renal cortical MDA （r=0. 817, P〈0.01 and r=0.547, P〈0.01, respectively）. The major manifestation of HCD-induced renal injury is apoptosis. The lipid peroxidation is a critical event to induce DNA damage and p53 is involved in the pathogenesis of lipid-induced renal injury.

关键词： hypercholesterolemia oxidative stress p53 apoptosis renal injury

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Adverse effects of triclosan on kidney in mice: Implication of lipid metabolism disorders

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Journal of Environmental Sciences 2023年第2期124卷 481-490页

作者： Wei Huang Guodong Cao Chengliang Deng Yanyan Chen Tao Wang Da Chen Zongwei Cai State Key Laboratory of Environmental and Biological Analysis Hong Kong Baptist UniversityHong Kong 999077China School of Environment Guangdong Key Laboratory of Environmental Pollution and HealthJinan UniversityGuangzhou 510632China Analysis Center School of PharmacyGuangdong Medical UniversityDongguan 523808China

Triclosan(TCS)is a ubiquitous antimicrobial used in daily consumer products.Previous reports have shown that TCS could induce hepatotoxicity,endocrine disruption,disturbance on immune function and impaired thyroid function.Kidney is critical in the elimination of toxins,while the effects of TCS on kidney have not yet been well-characterized.The aim of the present study was to investigate the effects of TCS exposure on kidney function and the possible underlying mechanisms in mice.Male C57BL/6 mice were orally exposed to TCS with the doses of 10 and 100 mg/(kg•day)for 13 weeks.TCS was dissolved in dimethyl sulfoxide(DMSO)and diluted by corn oil for exposure.Corn oil containing DMSO was used as vehicle control.Serum and kidney tissues were collected for study.Biomarkers associated with kidney function,oxidative stress,inflammation and fibrosis were assessed.Our results showed that TCS could cause renal injury as was revealed by increased levels of renal function markers including serum creatinine,urea nitrogen and uric acid,as well as increased oxidative stress,pro-inflammatory cytokines and fibroticmarkers in a dose dependent manner,whichweremore significantly in 100 mg/(kg•day)group.Mass spectrometry-based analysis of metabolites relatedwith lipid metabolism demonstrated the occurrence of lipid accumulation and defective fatty acid oxidation in 100 mg/(kg•day)TCS-exposed mouse kidney.These processes might lead to lipotoxicity and energy depletion,thus resulting in kidney fibrosis and functional decline.Taken together,the present study demonstrated that TCS could induce lipid accumulation and fatty acid metabolism disturbance in mouse kidney,whichmight contribute to renal function impairment.The present study further widens our insights into the adverse effects of TCS.

关键词： Triclosan renal injury Lipid accumulation Fatty acid oxidation

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Salvianolic acid A alleviates renal injury in systemic lupus erythematosus induced by pristane in BALB/c mice

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中国药理学与毒理学杂志 2016年第10期30卷 1039-1040页

作者： LIN Yi-huang YAN Yu ZHANG Hui-fang CHEN Yu-cai HE Yang-yang WANG Shou-bao FANG Lian-hua LYU Yang DU Guan-hua Beijing Key Laboratory of Drug Targets Identification and Drug Screening Institute of Materia MedicaChinese Academy of Medical Sciences and Peking Union Medical College State Key Laboratory of Cardiovascular Disease Fuwai Hospital National Center for Cardiovascular Diseases Beijing Key Laboratory of Polymorphic Drugs Institute of Materia MedicaChinese Academy of Medical Sciences and Peking Union Medical College

OBJECTIVE To investigate the effects of salvianolic acid A(SAA)in systemic lupus erythematosus(SLE)induced by pristane in BALB/c mice,this study was performed.METHODS Lupus mice were established by confirming elevated levels of autoantibodies and IL-6 after intraperitoneal injection of pristane.Micewere then treated with daily oral doses of SAA for 5months in parallel with mice treated with prednisone and aspirin as positive controls.The levels of autoantibodies were monitored at monthly intervals and nephritic symptoms observed by hematoxylin and eosin(H&E)and periodic acid-Schiff(PAS)staining.Western blot analysis of renal tissue was also employed.RESULTS SAA treatment caused a significant reduction in the levels of anti-Sm autoantibodies and reduced renal histopathological changes and pathological effects.SAA treatment also significantly inhibited the phosphorylation of IKK,IκB and NFκB in renal tissues of lupus mice.CONCLUSION The results suggest that SAA alleviates renal injury in pristane-induced SLE in BALB/c mice through inhibition of phosphorylation of IKK,IκB and NFκB.

关键词： salvianolic acid A systemic lupus erythematosus renal injury autoantibodies pristane NF-κB

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ELABELA protects against diabetic kidney disease by activating high glucose-inhibited renal tubular autophagy

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The Journal of Biomedical Research 2023年第6期37卷 460-469页

作者： Xiyin Zheng Lulu Yin Jing Song Juan Chen Wensha Gu Min Shi Hong Zhang Department of Endocrinology the Affiliated Huai'an No.1 People's Hospital of Nanjing Medical UniversityHuai'anJiangsu 223300China

ELABELA(ELA),an endogenous ligand of the apelin receptor(also known as apelin peptide jejunum[APJ]),has been shown to decrease in the plasma of patients with diabetic kidney disease(DKD).In the current study,we explored the potential function as well as the underlying mechanisms of ELA in DKD.We first found that the ELA levels were decreased in the kidneys of DKD mice.Then,we found that ELA administration mitigated renal damage and downregulated the expression of fibronectin,collagenⅣ,and transforming growth factor-β1 in the db/db mice and the high glucose cultured HK-2 cells.Furthermore,the autophagy markers,Beclin-1 and LC3-Ⅱ/LC3-Ⅰratio,were significantly impaired in DKD,but the ELA treatment reversed these alterations.Mechanistically,the inhibitory effects of ELA on the secretion of fibrosis-associated proteins in high glucose conditions were blocked by pretreatment with 3-methyladenine(an autophagy inhibitor).In summary,these in vivo and in vitro results demonstrate that ELA effectively protects against DKD by activating high glucose-inhibited renal tubular autophagy,potentially serving as a novel therapeutic candidate for DKD.

关键词： diabetic kidney disease ELABELA renal injury fibrosis renal tubular autophagy

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A review: Systematic research approach on toxicity model of liver and kidney in laboratory animals

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Animal Models and Experimental Medicine 2022年第5期5卷 436-444页

作者： Abbasali Abbasnezhad Fatemeh Salami Reza Mohebbati Department of Physiology Faculty of MedicineGonabad University of Medical SciencesGonabadIran Department of Physiology Faculty of MedicineMashhad University of Medical SciencesMashhadIran Applied Biomedical Research Center Mashhad University of Medical SciencesMashhadIran

Therapeutic experiments are commonly performed on laboratory animals to inves-tigate the possible mechanism(s)of action of toxic agents as well as drugs or sub-stances under consideration.The use of toxins in laboratory animal models,including rats,is intended to cause toxicity.This study aimed to investigate different models of hepatotoxicity and nephrotoxicity in laboratory animals to help researchers advance their research goals.The current narrative review used databases such as Medline,Web of Science,Scopus,and Embase and appropriate keywords until June 2021.Nephrotoxicity and hepatotoxicity models derived from some toxic agents such as cisplatin,acetaminophen,doxorubicin,some anticancer drugs,and other materials through various signaling pathways are investigated.To understand the models of renal or hepatotoxicity in laboratory animals,we have provided a list of toxic agents and their toxicity procedures in this review.

关键词： animal drug toxicity drug-induced abnormality liver dysfunction renal injury

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