小鼠受精素β亚单位真核表达载体pSG.SS.C3d3.YL-F_β构建及在HEK293细胞中的表达分析

目的:构建表达小鼠受精素β去整合素结构域(Fβ)的真核表达重组载体pSG.SS.C3d3.YL-Fβ,并对其在HEK293细胞中的表达进行分析。方法:应用PCR方法获得Fβ的cDNA片断,将其插入pSG.SS.C3d3.YL中,经酶切鉴定正确后转染HEK293细胞,并利用间接免疫荧光结合激光共聚焦技术、Western印迹技术、免疫组织化学染色技术及流式细胞仪检测技术对Fβ的表达进行检测。结果:成功构建了Fβ的真核表达重组载体pSG.SS.C3d3.YL-Fβ,该重组载体在HEK293细胞中能够表达Fβ。结论:Fβ在真核细胞中的成功表达为后续研究Fβ的高表达对受精过程的影响奠定了基础。     

表达肾癌G250基因和hGM-CSF基因HEK293细胞系的建立

目的 建立稳定表达肾癌G250基因与基因佐剂hGM-CSF基因编码蛋白的的HEK293细胞系。方法 通过脂质体转染的方法,将表达肾癌G250基因与细胞因子GM-CSF基因的双顺反子pIG250-GM真核表达质粒导入HEK293细胞中;经持续G418压力选择和有限稀释法获得稳定转染的细胞系;用免疫组化、ELISA和Western Blot方法,检测目的蛋白在HEK293细胞中的表达。结果 经600 μg/mL的G418压力筛选后,获得了抗性细胞克隆;免疫组织化学方法检测到表达G250的阳性细胞;ELISA方法检测到pIG250-GM转染组细胞培养上清中hGM-CSF的表达与空载体对照组比较,差异有统计学意义（P<0.05）;Western Blotting方法检测到G250蛋白的表达,分子量约54Ku,与预期大小相符。结论 成功建立可稳定表达肾癌G250基因与细胞因子GM-CSF基因的HEK293细胞系,为研究防治肾癌疫苗的免疫应答机制提供了实验基础。     

Renoprotective Effect of Spirulina fusiformis on Cisplatin-Induced Oxidative Stress and Renal Dysfunction in Rats

Cisplatin is an effective chemotherapeutic agent used in the treatment of a wide array of both pediatric and adult malignancies. Dose-dependent and cumulative nephrotoxicity is the major toxicity of this compound, sometimes requiring a reduction in dose or discontinuation of treatment. Recent evidences have implicated oxidative and nitrosative stress in cisplatin-induced nephrotoxicity. Spirulina fusiformis, blue-green algae, is claimed to be a potential antioxidant. The present study was designed to explore the renoprotective potential of Spirulina fusiformis against cisplatin-induced oxidative stress and renal dysfunction. Spirulina fusiformis (500,1000,1500 mg/kg^?1 p.o.) was administered 2 days before and until 3 days after cisplatin challenge (5 mg/kg^?1 i.p.). Renal injury was assessed by measuring serum creatinine, blood urea nitrogen, creatinine and urea clearance, and serum nitrite levels. Renal oxidative stress was determined by renal TBARS levels, reduced glutathione levels, and by enzymatic activity of superoxide dismutase and catalase. A single dose of cisplatin produced marked renal oxidative and nitrosative stress and significantly deranged renal functions. Chronic Spirulina fusiformis treatment significantly and dose-dependently restored renal functions, reduced lipid peroxidation, and enhanced reduced glutathione levels, superoxide dismutase, and catalase activities. The results of the present study clearly demonstrate the pivotal role of reactive oxygen species and their relation to renal dysfunction and point to the therapeutic potential of Spirulina fusiformis in cisplatin-induced nephrotoxicity.     

Stabilization of Oxidative Stress 1 Year after Kidney Transplantation: Effect of Calcineurin Immunosuppressives

Kidney transplantation (KT) is one of the best treatments for patients with chronic renal disease. It leads to improved kidney function, but the oxidative stress (OS) is only partially eliminated after KT. This study evaluated the effect of KT on outcomes, such as (a) specific kidney functions, (b) metabolic parameters, as well as (c) OS-related markers in 70 patients (46 males, 24 females; mean age = 54 ± 11) before and 1 year after KT. Post KT, the patients were divided into two groups: those receiving only cyclosporine A (N = 36) and those receiving only tacrolimus (N = 34). Improved kidney function (creatinine, urea, and glomerular filtration rate) and biochemical and hematological parameters were found 1 year after KT. OS-related markers (total antioxidant capacity, advanced oxidation protein, and lipid peroxidation products) decreased, but glutathione level increased after KT. Alterations in superoxide dismutase and catalase activities were also found. Glutathione peroxidase levels were unchanged. The level of oxidized low-density lipoprotein was surprisingly, not significantly increased. There was no significant difference between calcineurin inhibitors in any of the measured parameters. Improved renal function after KT is linked to reduction in OS but independent of immunosuppressive therapy.     

Effect of Intravenous Iron Sucrose on Oxidative Stress in Peritoneal Dialysis Patients

Aim. Intravenous iron therapy is an accepted treatment for patients receiving hemodialysis and continuous ambulatory peritoneal dialysis (CAPD). Studies have found enhanced oxidative stress in hemodialysis patients receiving intravenous iron, but there are no clinical data for CAPD patients. The aim of the current study was to investigate the effect of 100 mg of intravenous iron-sucrose on the erythrocyte (RBC) antioxidant enzymes (namely, superoxide dismutase [SOD], catalase [CAT], and glutathione peroxidase [GSHPx]) and plasma malondialdehyde (MDA), an oxidant molecule, in CAPD patients. Methods. Twelve CAPD patients receiving maintenance intravenous iron-sucrose were recruited. After a 12-hour fast, blood samples were taken for hemoglobin, iron, ferritin, and high-sensitivity C-reactive protein (hsCRP), and for baseline activities of erythrocyte antioxidant enzymes (i.e., SOD, CAT, GSHPx) and the plasma oxidant molecule, MDA. 100 mg iron-sucrose was infused over 30 minutes. Blood samples taken during (i.e., 15 minutes after commencement of infusion) and after (i.e., at 30 minutes, 60 minutes, and 6 hours after commencement) the infusion were taken for measurement of plasma iron, ferritin, TSAT, RBC SOD, CAT, GSHPx, and plasma MDA. Results. Plasma iron and transferrin saturation elevated significantly during infusion (p < 0.05). There was no significant change in erythrocyte SOD, CAT, GSHPx, or in MDA activities. There was a reduction of GSHPx activity at the 30th minute (from 153.69 ± 66.69 to 123.68 ± 25.50 mU/mL), but it was not statistically significant. The patients were grouped according to baseline ferritin (100–400 and 400–800 ng/mL); 60th-minute MDA was significantly higher in the latter group (p < 0.05). There was no correlation between hsCRP and oxidant-antioxidant balance. No correlation was noted between RBC antioxidant enzymes or plasma oxidant molecule and ferritin levels. Conclusion. There are no acute deteriorating effects from a 100 mg of intravenous iron-sucrose in CAPD patients with optimal iron stores. This dose may be applied safely in CAPD patients.     

Association of Superoxide-Induced Oxidative Stress With Rotator Cuff Tears in Human Patients

Rotator cuff degeneration is one of the factors contributing to rotator cuff tears. Oxidative stress is involved in tendon degeneration, and superoxide-induced oxidative stress plays a pathological role in regulating the balance between oxidation and reduction. The role of oxidative stress in rotator cuff tears, however, is unclear. This study, therefore, aimed to investigate the contribution of superoxide-induced oxidative stress to rotator cuff tears. Seventy patients were recruited and divided into two groups: patients with (Ruptured group) and those without (Unruptured group) a rotator cuff tear. Specimens from both groups were collected during surgery. Degeneration morphology was classified according to the degeneration score. Superoxide-induced oxidative stress was assessed according to dihydroethidium (DHE) relative fluorescence intensity, capacity for antioxidation according to superoxide dismutase (SOD) activity, and the balance between oxidation and reduction based on the redox ratio. Data were compared between groups. Correlations between the degeneration score and the oxidative stress factors were calculated. Degeneration score and DHE relative fluorescence intensity were significantly higher in the Ruptured than the Unruptured group. The SOD activity was not significantly different between groups. Degeneration score was positively correlated with both DHE relative fluorescence intensity and SOD activity. Thus, superoxide-induced oxidative stress and tendon degeneration were greater in rotator cuff tear tissues than in those with no tear, suggesting that oxidative imbalance may be involved in degenerative rotator cuff tears. Clinical Relevance: Understanding the mechanisms of superoxide-induced oxidative stress may lead to targeted tissue therapy for degenerative rotator cuff tears. © 2019 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 38:212–218, 2020     

Early Events in Kidney Donation: Progression of Endothelial Activation, Oxidative Stress and Tubular Injury After Brain Death

Cerebral injury leading to brain death (BD) causes major physiologic derangements in potential organ donors, which may result in vascular-endothelial activation and affect posttransplant graft function. We investigated the kinetic of pro-coagulatory and pro-inflammatory endothelial activation and the subsequent oxidative stress and renal tubular injury, early after BD declaration. BD was induced by slowly inflating a balloon-catheter inserted in the extradural space over a period of 30 min. Rats (n = 30) were sacrificed 0.5, 1, 2 or 4 h after BD-induction and compared with sham-controls. This study demonstrates immediate pro-coagulatory and pro-inflammatory activation of vascular endothelium after BD in kidney donor rats, proportional with the duration of BD. E- and P-Selectins, Aα/Bβ-fibrinogen mRNA were abruptly and progressively up-regulated from 0.5 h BD onwards; P-Selectin membrane protein expression was increased; fibrinogen was primarily visualized in the peritubular capillaries. Plasma von Willebrand factor was significantly higher after 2 h and 4 h BD. Urine heart-fatty-acid-binding-protein and N-acetyl-glucosaminidase, used as new specific and sensitive markers of proximal and distal tubular damage, were found significantly increased after 0.5 h, with a maximum at 4 h. Unexpectedly, oxidative stress was detectable only late, after the installation of tubular injury, suggesting only a secondary role for hypoxia in triggering these injuries.     

Renoprotective Effect of Grape Seed Extract against Oxidative Stress Induced by Gentamicin and Hypercholesterolemia in Rats

Abstract

Rationale: Kidneys are dynamic organs and represent one of the major systems maintaining the body homeostasis; they are affected by many chemicals and drugs. Grape seed extract (GSE) has been targeted to prevent drug-induced renal toxicity. Objectives: This study investigates the possible renoprotective effect of GSE against oxidative stress, renal impairment, and hypercholesterolemia (HC) induced by gentamicin (GM) and cholesterol-enriched diet. Seventy adult male Wistar rats (160 ± 10 g) were divided into seven groups: (1) served as control, (2) GSE, (3) GM, (4) GSE + GM, (5) hypercholesterolemic (HC) group, (6) GM + HC group, and (7) GM + HC + GSE. Kidney functions, inflammatory mediators, cytokines, lipid profile, nitric oxide (NO), cyclic guanosine monophosphate (cGMP), and oxidative and antioxidative stress parameters were assessed in all groups. Main findings: GM induced renal dysfunction, which was exacerbated by the presence of HC as confirmed by laboratory determinations. Administration of GSE attenuated the renal toxicity evidenced in significant reduction in elevated kidney function, inflammatory cytokines as well as lipid profile, NO, cGMP, enzymatic, and nonenzymatic antioxidants. Conclusion: Administration of GSE simultaneously with GM attenuated oxidative stress, diminished renal toxicity, and improved lipid profile induced by GM and HC.     

Acute Effect of Standard Heparin Versus Low Molecular Weight Heparin on Oxidative Stress and Inflammation in Hemodialysis Patients

Objective. Atherosclerotic cardiovascular diseases caused by traditional and non-traditional risk factors are the most common cause of morbidity and mortality in hemodialysis patients. Recently, much interest has been focused on non-traditional factors, such as oxidative stress, inflammation, and endothelial dysfunction. Hemodialysis patients are not only exposed to oxidative stress but also to inflammation. Although anticoagulants are the most frequently used drugs in hemodialysis patients, their effect upon oxidative stress and inflammation in dialysis patients are still unknown. Methods. Thirty-three hemodialysis patients were randomized into three groups. Group 1 received standard heparin while group 2 received low molecular weight heparin during the dialysis therapy. Group 3 (control group) did not receive any anticoagulant agent. Investigators were blinded to the therapy. Serum concentrations of oxidative stress and inflammation markers, including C-reactive protein, tumor necrosis factor alpha, superoxide dismutase, and malondialdehyde, were measured before and after dialysis session. Results. The oxidative stress and inflammation markers were significantly increased in groups 1 and 3 (p < 0.05 for each) compared to their baseline values. In contrast, baseline and end-treatment values of the oxidative stress and inflammation markers were comparable in the group 2 (p > 0.05). Conclusion. These findings indicate that the type of anticoagulants may take a role in the acute effect of hemodialysis upon oxidative stress and inflammation markers. A comparison of the groups revealed that low molecular weight heparin decreased the oxidative stress and inflammation, whereas standard heparin increased the oxidative stress and inflammation. Low molecular weight heparin appears to have an additive benefit for hemodialysis patients.     

邻苯二甲酸二丁酯对大鼠精子运动能力及氧化应激的影响

目的 :探讨邻苯二甲酸二丁酯 (DBP)对大鼠睾丸抗氧化系统和精子运动能力的影响。　方法 :将 6周龄雄性SD大鼠随机分成 0 (对照组 )、2 5 0、5 0 0、10 0 0mg/(kg·d) 4组 ,每组 8只 ,灌胃给予DBP ,共染毒 4周。用计算机辅助精子分析系统 (CASA)观察附睾尾部精子运动速度参数 :曲线运动速度 (VCL)、直线运动速度 (VSL)、平均路径速度 (VAP)、鞭打频率 (BCF)和精子运动方式参数 :精子头侧摆幅度 (ALH)、直线性 (LIN)、平均移动角度 (MAD)、前向性 (STR)的变化。用分光光度法测定血清和睾丸匀浆中超氧化物歧化酶 (SOD)活力和丙二醛 (MDA)含量 ,同时观察每日体重增加量及肝、睾丸、附睾等脏器系数的变化。　结果 :染毒后肝脏器系数显著上升 ,各剂量组与对照组相比差异均有显著性 (P <0 .0 1) ;睾丸脏器系数下降 ,10 0 0mg/(kg·d)组与对照组相比P <0 .0 1;VCL、ALH随染毒剂量的增加呈下降趋势 ,10 0 0mg/(kg·d)组与对照组相比差异均有显著性 (P <0 .0 5 ) ;睾丸匀浆SOD活力降低 ,10 0 0mg/(kg·d)组与对照组相比差异有显著性 (P <0 .0 5 ) ;其他指标的改变差异无显著性。　结论 :DBP可引起大鼠睾丸精子运动能力和抗氧化能力的下降。睾丸是DBP毒作用的主要靶器官之一。     

Oxidative Stress in 5/6 Nephrectomized Rat Model: Effect of Alpha-Lipoic Acid

Alpha-lipoic acid (ALA) is a powerful antioxidant, and its effect in ameliorating complications of diabetes mellitus has been widely documented. The aim of this study was to investigate the role of ALA in the disease progression of remnant kidneys (RK). Systolic blood pressure (SBp), hemoglobin, renal function, kidney malondialdehyde (MDA), glutathione (GSH), vitamin E (Vit E) concentrations, p65 nuclear factor (NF)-κB activity, and macrophage infiltration were analyzed in sham and RK rats supplemented with ALA (100 mg/kg body weight, i.p., every other day) or vehicle for 12 weeks. RK rats exhibited increases in SBp, kidney MDA concentration, p65 NF-κB activity, and macrophage infiltration, which were prominent in weeks 4 and 8 and decreased at week 12. RK rats also showed anemia, microalbuminuria, and decreased renal function and kidney GSH and Vit E concentrations. These changes were all attenuated by 8 weeks of ALA treatment compared to RK vehicle group. But the continued ALA treatment after week 8 reversed the beneficial effect on SBp, kidney MDA concentration, p65 NF-κB activity, macrophage infiltration, anemia, microalbuminuria, and renal function, while the beneficial effect was maintained if the treatment was discontinued after week 8. Furthermore, ALA increased albuminuria and kidney MDA concentration in sham animals. In conclusion, ALA administration attenuates oxidative stress, inflammation, and hypertension and delayed the deterioration of kidney function in RK rats with enhanced oxidative stress, while in healthy animals or RK rats with a well-balanced redox state, ALA may act as a pro-oxidant, contributing to renal dysfunction.     

Effect of curcumin on cisplatin- and oxaliplatin-induced oxidative stress in human embryonic kidney (HEK) 293 cells

Generation of reactive oxygen species (ROS) is involved in the nephrotoxicity of platinum anticancer drugs. This study involved incubation of human embryonic kidney (HEK) 293 cells in cell culture media supplemented with cisplatin or oxaliplatin in the presence or absence of curcumin, a well-studied antioxidant. Thereafter several indices of oxidative stress have been measured, which included glutathione (GSH), total antioxidant capacity (TAC), and antioxidant enzymes [(superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidases (GPX)]. The impact of platinum drugs on cells viability, lipid peroxidation, and lactate dehydrogenase leakage was also examined. The results show that at both acute (60 min) and chronic (24 h) durations of incubation, cisplatin and oxaliplatin induced oxidative stress as evidenced by significant inhibition of the activities of SOD, CAT, and GPX enzymes as well as significant reduction of the concentrations of GSH and TAC. Curcumin ameliorated the oxidative stress induced by these insults by significantly restoring the measured oxidative indices. Our findings provide evidence that curcumin significantly ameliorates oxidative stress induced by both cisplatin and oxaliplatin in HEK cells.     

Epithelial-to-Mesenchymal Transdifferentiation of Renal Tubular Epithelial Cell Mediated by Oxidative Stress and Intervention Effect of Probucol in Diabetic Nephropathy Rats

Objective: To elucidate the relationship of oxidative stress and specificity protein 1 (Sp1) in the process of epithelial-to-mesenchymal transdifferentiation (EMT) and also to investigate the molecular mechanism of protective effect of probucol on the pathogenesis of diabetic kidney disease (DKD). Methods: Thirty male Sprague–Dawley (SD) rats were randomly divided into control group, diabetic group, and diabetic group under probucol therapy (n = 10 per group). The biochemical indicators including 24-h urinary total protein (24-h UTP) excretion, blood glucose (BG), lipids [triglycerides (TGs), total cholesterol (TC)], serum creatinine (Scr), creatinine clearance rate (Ccr), kidney tissue malondialdehyde (MDA) level, and glutathione peroxidase (GSH-Px) activity were assessed in all groups. The renal pathological changes were evaluated by hematoxylin and eosin (HE) and Masson staining. The protein expression of Sp1, α-smooth muscle actin (α-SMA), and E-cadherin was also measured and analyzed by immunohistochemistry and Western blotting. Results: Compared with the control group, the BG, TC, Scr, 24-h UTP, and MDA level of renal tissue increased significantly and the Ccr reduced in the rats of diabetic group (all p < 0.01). The pathological scores and the expression of Sp1 and α-SMA in renal tissue were up-regulated (p < 0.01) and the expression of E-cadherin was down-regulated significantly in the diabetic animals (p < 0.01). In the diabetic animals treated with probucol, the renal injuries were alleviated (p < 0.01). Conclusions: Oxidative stress may play an important role in the EMT process of tubular epithelial cells. Probucol could ameliorate renal disease progression in this model of diabetic nephropathy, which might be due to an antioxidant action, down-regulation of Sp1 protein expression, and inhibition of renal tubular EMT.     

Taurine ameliorates cytotoxic effects of Di(2-ethylhexyl) phthalate on Leydig cells

It has been revealed that di(2-ethylhexyl)phthalate (DEHP) has toxic impacts on the male reproductive system. Taurine (TAU) is an amino acid with antioxidant property and beneficial impacts on the male reproductive system. In this study, protective impacts of Taurine (TAU) on DEHP-induced Leydig TM3 cell toxicity were investigated. The cells exposed to DEHP (0.8 µmol) or TAU (100 mg/ml) for 24 hr. Cell viability (MTT assay), apoptosis, oxidative stress and testosterone level were examined. DEHP could significantly decrease the cell viability percentage, reduce testosterone level, increase apoptosis, elevate Bax/ Bcl-2 ratio and enhance caspase-3 and -9 activity in the TM3 cells. Additionally, DEHP significantly elevated malondialdehyde contents and reactive oxygen species levels. It also augmented superoxide dismutase and catalase activity in the Leydig cells. Co-treatment of DEHP with TAU increased viability and testosterone level, while oxidative stress and apoptosis significantly reduced. TAU could decrease Bax/Bcl-2 ratio and caspase-3 and -9 activity in the DEHP-intoxicated cells. Our results have clearly shown that TAU protects TM3 cells against oxidative stress and apoptosis induced by DEHP.     

Advanced Oxidation Protein Products Induce Vascular Calcification by Promoting Osteoblastic Trans-Differentiation of Smooth Muscle Cells via Oxidative Stress and ERK Pathway

Vascular calcification is an actively regulated process similar to bone formation. Advanced oxidation protein products (AOPPs) have been demonstrated to be novel markers of oxidant-mediated protein damage. The present study investigated the role of AOPPs in inducing osteoblastic trans-differentiation and calcification of smooth muscle cells in vitro. We found that AOPPs directly increased the calcium deposition and expression of core binding factor-α1 (CBF-α1) and osteopontin (OPN) and significantly decreased SM-α-actin expression in human aortic smooth muscle cells (HASMCs). AOPPs increased intracellular oxidative stress, which was inhibited by vitamin E. Vitamin E also inhibited AOPP-induced calcium content and osteoblast differentiation of HASMCs. Furthermore, the inhibitor of ERK significantly suppressed the effects of AOPPs on calcification and osteoblast marker expression. These findings suggest that AOPPs induce vascular calcification by promoting osteoblast differentiation of smooth muscle cells via oxidative stress and ERK pathway.     

Assessment of Matrix Gla Protein,Klotho Gene Polymorphisms,and Oxidative Stress in Chronic Kidney Disease

Abstract

Increased vascular calcification and oxidative stress are considered as extra renal risk factors at the pathogenesis cardiovascular events in chronic kidney disease (CKD). We investigated matrix Gla protein (MGP) (T-138C, Glu60X, Thr83Ala) and Klotho (Cys370Ser) gene polymorphisms, serum MGP levels, and oxidative stress status of 84 CKD patients and 37 healthy controls. The MGP gene Glu60X and Thr83Ala polymorphisms were significantly associated with CKD. The correlation between T-138C genotype of MGP gene, Cys370Ser genotype of Klotho gene, and CKD was not significant (p > 0.05). At the haplotype analysis, the combination of the X allele of Glu60X and the Thr allele of Thr83Ala showed a significantly increased risk of CKD (p < 0.05). X allele, Thr allele, and C allele of T-138C were associated with diabetes mellitus and CKD phenotypes occurring concurrently (p < 0.01). Serum zinc levels were significantly low in end-stage renal disease (ESRD) patients (p = 0.0001). The total comet score frequency of ESRD patients was higher than that of control group (p < 0.05). The urinary 8-hydroxy-2′-deoxyguanosine levels were significantly high in CKD patients (p < 0.05). According to this study, analyzing the distribution of MGP gene and oxidative stress status would be very informative in order to detect their role at CKD.     

Effect of Chenodeoxycholic Acid on Fibrosis, Inflammation and Oxidative Stress in Kidney in High-Fructose-Fed Wistar Rats

Background: Recent studies indicate farnesoid X receptor (FXR) plays an important role in regulating lipid metabolism in kidney disease. The purpose of the present study is to investigate the effect of chenodeoxycholic acid (CDCA), a FXR agonist, on fibrosis, inflammation and oxidative stress in kidney in rats fed on high fructose. Methods: Twenty-four healthy male Wistar rats were randomly divided into three groups (n=8): normal control group, high fructose group and chenodeoxycholic acid group. Rats were sacrificed by the end of 16 weeks after feeding. Blood urea nitrogen, serum creatinine, fast glucose, lipid concentration were observed, spot urine samples were obtained to measure the albumin and creatinine levels. Triglyceride of renal cortices was detected. The mRNA level and protein contents of the fibrosis-inducing growth factor transforming growth factor β1 (TGF-β1) and plasminogen activator inhibitor (PAI-I), inflammatory cytokines tumor necrosis factor α (TNF-α) and interleukin 6 (IL-6), oxidative stress index NADPH oxidase 2 (Nox2) and p22phox in kidney were examined. The pathological changes of kidney were examined by PAS staining and immunohistochemical staining. Electron microscope sections were made to measure glomerular basement membrane (GBM) width. Results: Renal injuries including mesangial expansion, GBM thickness and podocyte foot process effacement were found in fructose-fed Wistar rats, FXR agonist CDCA modulates renal lipid metabolism, decreases proteinuria and improves renal fibrosis, inflammation and oxidation stress. High-fructose-feeding may cause lipid nephrotoxicity through down-regulated farnesoid X receptor and increases expression of profibrotic growth factors, proinflammatory cytokines, and oxidative stress in Wistar rats. Conclusion: FXR activation by chenodeoxycholic acid can prevent the injury in kidney induced by high fructose feeding.