scholarly journals Oxidative stress-induced c-Jun N-terminal kinase (JNK) activation in tendon cells upregulates MMP1 mRNA and protein expression

2007 ◽  
Vol 25 (3) ◽  
pp. 378-389 ◽  
Author(s):  
Fang Wang ◽  
George A.C. Murrell ◽  
Min-Xia Wang
Keyword(s):  
Oxidative Stress ◽  
Protein Expression ◽  
Tendon Cells ◽  
Mrna And Protein Expression ◽  
Jnk Activation

scholarly journals Se Alleviated Oxidative Stress-Mediated Complex Poisoning Mechanism in Pb-Treated Chicken Kidneys: Inflammation, Heat Shock Response, and Autophagy

2021 ◽  
Author(s):  
Zhiying Miao ◽  
Weikang Yu ◽  
Yueyang Wang ◽  
Xianhong Gu ◽  
Xiaohua Teng
Keyword(s):  
Oxidative Stress ◽  
Heat Shock ◽  
Protein Expression ◽  
Heat Shock Response ◽  
Potable Water ◽  
Histological Structure ◽  
Standard Diet ◽  
Shock Response ◽  
Mrna And Protein Expression ◽  
Shock Proteins

Abstract Background: Lead (Pb) is a toxic environmental pollutant and can exerts toxicity in kidneys. It is known that selenium (Se) has an antagonistic effect on Pb poisoning. However, biological events during the process were not well understood in chicken kidneys.Methods: One hundred and eighty male Hyline chickens (7-day-old) were randomly divided into the control group (offering standard diet and potable water), the Se group (offering Na2SeO3-added standard diet and potable water), the Pb group (offering standard diet and (CH3OO)2Pb-added potable water), and the Pb+Se group (offering Na2SeO3-added standard diet and (CH3OO)2Pb-added potable water). On 30th, 60th, and 90th days, kidneys were removed to perform the studies of histological structure, oxidative stress indicators, cytokines, heat shock proteins, and autophagy in the chicken kidneys.Results: The experimental results indicated that Pb poisoning changed renal histological structure; decreased catalase, glutathione-s-transferase, and total antioxidative capacity activities; increased hydrogen peroxide content; induced mRNA and protein expression of heat shock proteins; inhibited interleukin (IL)-2 mRNA expression, and induced IL-4 and IL-12β mRNA expression; inhibited mammalian target of rapamycin mRNA and protein expression, and induced autophagy-related gene mRNA and protein expression in the chicken kidneys. Supplement of Se mitigated the above changes caused by Pb.Conclusion: Our research strengthens the evidence that Pb induced oxidative stress, inflammation, heat shock response, and autophagy and Se administration alleviated Pb poisoning through mitigating oxidative stress in the chicken kidneys.

scholarly journals Effect of Different Exercise Loads on Testicular Oxidative Stress and Reproductive Function in Obese Male Mice

2020 ◽  
Vol 2020 ◽  
pp. 1-13 ◽  
Author(s):  
Xuejie Yi ◽  
Donghui Tang ◽  
Shicheng Cao ◽  
Tao Li ◽  
Haining Gao ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Protein Expression ◽  
Sperm Quality ◽  
Reproductive Function ◽  
High Load ◽  
Serum Testosterone Level ◽  
Male Mice ◽  
Male Reproductive Function ◽  
Mrna And Protein Expression ◽  
Moderate Load

This study is aimed at investigating the effect of different exercise loads on the reproductive function of obese male mice and the underlying mechanisms. Male mice with high-fat diet-induced obesity were divided into obesity control (OC), obesity moderate-load exercise (OME), and obesity high-load exercise (OHE) groups. The OME and OHE groups were subjected to swimming exercise 5 days per week over a duration of 8 weeks, with the exercise load progressively increased to 2 h per day in the OME group and 2 h twice per day in the OHE group. In the OC group mice without exercise regimen, we observed a decrease in mRNA expression of antioxidant enzymes, increase in free radical products, upregulation of mRNA and protein expression of nuclear factor-κB and proinflammatory cytokines, inhibition of mRNA and protein expression of testosterone synthases, decrease in the serum testosterone level and sperm quality, and increase in sperm apoptosis. Although both moderate-load exercise and high-load exercise reduced body fat, only moderate-load exercise effectively alleviated obesity-induced oxidative stress, downregulated the expression of nuclear factor-κB and proinflammatory cytokines, and reversed the decrease in mRNA and protein expression of testosterone synthases, serum testosterone level, and sperm quality. These changes were not observed in the OHE group mice. Obesity-induced testicular oxidative stress and inflammatory response decreased testosterone synthesis and sperm quality. Moderate-load exercise alleviated the negative effect of obesity on male reproductive function by decreasing testicular oxidative stress and inflammatory responses. Although high-load exercise effectively reduced body fat, its effects on alleviating oxidative stress and improving male reproductive function were limited.

scholarly journals Proanthocyanidins Alleviates AflatoxinB1-Induced Oxidative Stress and Apoptosis through Mitochondrial Pathway in the Bursa of Fabricius of Broilers

Toxins ◽  
2019 ◽  
Vol 11 (3) ◽  
pp. 157 ◽  
Author(s):  
Shahid Rajput ◽  
Cong Zhang ◽  
Yue Feng ◽  
Xiao Wei ◽  
Mahmoud Khalil ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Enzymes ◽  
Protein Expression ◽  
Basal Diet ◽  
Mitochondrial Pathway ◽  
Bursa Of Fabricius ◽  
Enzymes Activities ◽  
Study Results ◽  
Mrna And Protein Expression ◽  
Antioxidant Enzymes Activities

Aflatoxin B1 (AFB1) is a serious threat to the poultry industry. Proanthocyanidins (PCs) demonstrates a broad range of biological, pharmacological, therapeutic, and chemoprotective properties. The aim of this study was to investigate the ameliorative effects of PCs against AFB1-induced histopathology, oxidative stress, and apoptosis via the mitochondrial pathway in the bursa of Fabricius (BF) of broilers. One hundred forty-four one-day old Cobb chicks were randomly assigned into four treatment groups of six replicates (6 birds each replicate) for 28 days. Groups were fed on the following four diets; (1) Basal diet without addition of PCs or AFB1 (Control); (2) basal diet supplemented with 1 mg/kg AFB1 from contaminated corn (AFB1); (3) basal diet supplemented with 250 mg/kg PCs (PCs); and (4) basal diet supplemented with 1 mg/kg AFB1 + 250 mg/kg PCs (AFB1+ PCs). The present study results showed that antioxidant enzymes activities of total superoxide dismutase (T-SOD), catalase (CAT), glutathione peroxidase (GSH-Px), and glutathione S-transferase (GST) in AFB1 treated group were (p < 0.05) decreased, whereas malondialdehyde (MDA) contents were significantly increased in comparison with the control group. Furthermore, we found that dietary PCs treatment ameliorated AFB1-induced oxidative stress in the BF through inhibiting the accumulation of MDA content and enhancing the antioxidant enzymes activities (T-SOD, CAT, GSH-Px, and GST). Similarly, PCs markedly enhanced messenger RNA (mRNA) expression of antioxidant genes (SOD, CAT, GPx1, and GST) in comparison with AFB1 group. Moreover, histological results showed that PCs alleviated AFB1-induced apoptotic cells in the BF of broilers. In addition, both mRNA and protein expression results manifested that mitochondrial-apoptosis-associated genes (Bax, caspase-9, caspase-3, and p53 and cytochrome c) showed up-regulation, while (Bcl-2) showed down-regulation in AFB1 fed group. The supplementation of PCs to AFB1 diet significantly reversed the mRNA and protein expression of these apoptosis-associated genes, as compared to the AFB1 group. Our results demonstrated that PCs ameliorated AFB1-induced oxidative stress by modulating the antioxidant defense system and apoptosis in the BF through mitochondrial pathway in broilers.

miR-673/menin/JunD axis modulates hyperglycemia-induced oxidative stress and inflammation in the diabetic heart

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
R Suades ◽  
S Hussain ◽  
A.W Khan ◽  
S Costantino ◽  
F Paneni ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Transcription Factor ◽  
Protein Expression ◽  
Myocardial Dysfunction ◽  
Reactive Oxygen Species Generation ◽  
Left Ventricular ◽  
Diabetic Heart ◽  
Lv Function ◽  
Funding Source ◽  
Mrna And Protein Expression

Abstract Background Hyperglycemia-induced reactive oxygen species generation in diabetic heart contributes to myocardial dysfunction. JunD, a member of the activated protein 1 (AP-1) family of transcription factors, is emerging as a major gatekeeper against oxidative stress. Previous studies have shown that downregulation of AP-1 transcription factor JunD is involved in vascular aging and heart failure. However, the role of JunD in diabetes-induced myocardial dysfunction is unknown. Purpose The present study was designed to investigate whether hyperglycemia-driven epigenetic regulation of JunD contributes to oxidative stress, inflammation and myocardial dysfunction in the diabetic heart. Methods Diabetes (DB) was induced in C57BL/6 wild-type (WT) mice by streptozotocin. After four weeks of DB, left ventricular (LV) function was assessed by standard and 2D speckle-tracking echocardiography in both groups (n=10). Then, the animals were euthanized and LV specimens were collected to determine JunD mRNA and protein expression as well as superoxide anion production by ESR spectroscopy. Chromatin modifications of JunD gene promoter were assessed by chromatin immunoprecipitation. Isolated DNA was analyzed for promoter methylation following Methylminer kit. Cardiac biopsies were collected from age-matched patients with and without diabetes. Results DB mice showed LV dysfunction with reduced ejection fraction and fractional shortening. JunD mRNA and protein expression were reduced in the myocardium of DB as compared to control mice. JunD downregulation was associated with oxidative stress, increased NF-kB binding activity and expression of inflammatory mediators. Accordingly, expression of free radical scavenger superoxide dismutase 1 and aldehyde dehydrogenase 2 was reduced, whereas nicotinamide adenine dinucleotide phosphate oxidase subunits NOX2 and NOX4 were upregulated in DB. A reduction of JunD mRNA and protein expression was confirmed in LV specimens obtained from patients with diabetes. The downregulation of JunD was epigenetically regulated by promoter hypermethylation and histone modifications. Post-translational repression by tumor suppressor menin also contributed to JunD downregulation. Indeed, menin was significantly upregulated in DB hearts and co-immunoprecipitation experiments confirmed the binding of menin to JunD. Furthermore, rat ventricular myocytes exposed to high glucose (HG) showed increased menin expression. We found that miR-673 targeting menin was downregulated in hearts of DB mice. Reprogramming miR-673 in HG-treated myocytes was able to restore both menin and JunD expression to control levels. Conclusions Our findings show that downregulation of AP-1 transcription factor JunD contributes to diabetes-induced myocardial dysfunction and miR-673/menin/JunD represents a novel molecular axis involved in hyperglycemia-induced ROS-driven cardiac damage. Funding Acknowledgement Type of funding source: Foundation. Main funding source(s): European Society of Cardiology (ESC) Research Grant 2017

scholarly journals Hepatic Postnatal Developmental Expression of Trace Mineral Associated Antioxidant Enzymes

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 1077-1077
Author(s):  
Laura Sherlock ◽  
Kara Sjostrom ◽  
Nancy Krebs ◽  
Clyde Wright ◽  
Eva Nozik-Grayck
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Enzymes ◽  
Protein Expression ◽  
Developmental Regulation ◽  
Immune Surveillance ◽  
Developmental Expression ◽  
Antioxidant Defenses ◽  
Trace Mineral ◽  
Mrna And Protein Expression ◽  
Neonatal Liver

Abstract Objectives Oxidative stress is central to the etiology of many diseases of prematurity. Lower antioxidant defenses render premature infants vulnerable to oxidative damage secondary to infection and oxygen therapy. Antioxidant enzymes (AOE) increase perinatally in the blood and lungs. Many AOE require a micronutrient such as selenium (Se) or zinc (Zn) to function at maximum efficacy. These trace elements are low in neonates compared to adults. The liver is an important immune surveillance organ where antioxidant defense is critical for host response. It also plays a major role in micronutrient processing. However, the developmental regulation and expression of AOE in the liver is incompletely described. We hypothesized the neonatal liver would have decreased trace mineral associated AOE. Methods C57BL/6mice were sacrificed at P0, P7, P21 and 8–12 weeks. mRNA and protein expression of key AOE (SOD1, SOD2, SOD3, Gpx1, Gpx4, Msrb1, TrxR1) and factors for Se processing (Sephs2/Sps2, Scly, Pstk) were measured by qPCR and Western blot. Results Hepatic mRNA for selenoenzymes Gpx1 and Msrb1 were developmentally regulated, low at P0 and increased by adult (P &lt; 0.05, n = 5–6). Gpx1 protein increased 7–8-fold and Msrb1 protein increased 6-fold from P0 to adult (P &lt; 0.0001, n = 4). Gene expression of Zn related SOD1 and Mn SOD2 increased postnatally, low at P0 and increased in adult (P &lt; 0.01 n = 5–6). Protein expression for each increased 1.5 and 3-fold from P0 to adult respectively (P &lt; 0.001, n = 4) The mRNA and protein expression for Gpx4, TrxR1 and SOD3 remained constant postnatally. As the greatest increase was observed in selenoenzymes, factors for Se processing were evaluated. Sephs2, Scly and Pstk mRNA increased from P0 compared to P21 and adult mice (P &lt; 0.05, n = 4–6). Protein expression for Pstk and Scly was highest at P21 and protein for Sps2 increased postnatally (P &lt; 0.01, n = 4). Conclusions The liver experiences a postnatal increase in essential trace mineral associated AOE. Additionally, the hepatic machinery for Se processing is low in neonatal mice. We speculate that the neonatal liver is vulnerable to oxidative stress secondary to low AOE defense. We also speculate states that decreased neonatal micronutrient status may further impair the hepatic redox state. Funding Sources CCTSI Child Maternal Health Mentored Grant (L.S).

Oxidative stress activates anion exchange protein 2 and AP-1 in airway epithelial cells

2002 ◽  
Vol 283 (4) ◽  
pp. L791-L798 ◽  
Author(s):  
Jennifer L. Turi ◽  
Ilona Jaspers ◽  
Lisa A. Dailey ◽  
Michael C. Madden ◽  
Luisa E. Brighton ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Epithelial Cells ◽  
Protein Expression ◽  
Anion Exchange ◽  
Airway Epithelial Cells ◽  
Airway Epithelial ◽  
Anion Exchange Protein ◽  
Mrna And Protein Expression ◽  
Exchange Protein

Anion exchange protein 2 (AE2) is a membrane-bound protein that mediates chloride-bicarbonate exchange. In addition to regulating intracellular pH and cell volume, AE2 exports superoxide (O[Formula: see text]·) to the extracellular matrix in an HCO[Formula: see text]-dependent process. Given this ability to export O[Formula: see text]·, we hypothesized that expression of AE2 in the lung is regulated by oxidative stress. AE2 mRNA and protein expression was measured by RT-PCR and Western blot analysis, respectively, in differentiated human bronchial epithelial cells exposed to H2O2 (100 μM). Alterations in in vivo AE2 protein expression were evaluated in lung tissue of rats exposed to 70% O2. The role of transcription factor activator protein (AP)-1 in oxidant regulation of AE2 was evaluated by EMSA and by immunoblotting of nuclear phospho-c- jun. Results show increased AE2 mRNA and protein expression after oxidant exposure. This was preceded by transient increases in DNA binding of AE2-specific AP-1 and phosphorylation of c- jun. This study demonstrates that AE2 expression is regulated by oxidative stress in airway epithelial cells and that this regulation correlates with activation of AP-1.

scholarly journals Hyperglycemia Induces Myocardial Dysfunction via Epigenetic Regulation of JunD

2020 ◽  
Vol 127 (10) ◽  
pp. 1261-1273
Author(s):  
Shafaat Hussain ◽  
Abdul Waheed Khan ◽  
Alexander Akhmedov ◽  
Rosa Suades ◽  
Sarah Costantino ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Diabetes Mellitus ◽  
Reactive Oxygen Species ◽  
Protein Expression ◽  
Cardiac Dysfunction ◽  
Nicotinamide Adenine Dinucleotide ◽  
Myocardial Dysfunction ◽  
Left Ventricular ◽  
Oxygen Species ◽  
Mrna And Protein Expression

Rationale: Hyperglycemia -induced reactive oxygen species are key mediators of cardiac dysfunction. JunD (Jund proto-oncogene subunit), a member of the AP-1 (activator protein-1) family of transcription factors, is emerging as a major gatekeeper against oxidative stress. However, its contribution to redox state and inflammation in the diabetic heart remains to be elucidated. Objective: The present study investigates the role of JunD in hyperglycemia-induced and reactive oxygen species–driven myocardial dysfunction. Methods and Results: JunD mRNA and protein expression were reduced in the myocardium of mice with streptozotocin-induced diabetes mellitus as compared to controls. JunD downregulation was associated with oxidative stress and left ventricular dysfunction assessed by electron spin resonance spectroscopy as well as conventional and 2-dimensional speckle-tracking echocardiography. Furthermore, myocardial expression of free radical scavenger superoxide dismutase 1 and aldehyde dehydrogenase 2 was reduced, whereas the NOX2 (NADPH [nicotinamide adenine dinucleotide phosphatase] oxidase subunit 2) and NOX4 (NADPH [nicotinamide adenine dinucleotide phosphatase] oxidase subunit 4) were upregulated. The redox changes were associated with increased NF-κB (nuclear factor kappa B) binding activity and expression of inflammatory mediators. Interestingly, mice with cardiac-specific overexpression of JunD via the α MHC (α- myosin heavy chain) promoter (α MHC JunD tg ) were protected against hyperglycemia-induced cardiac dysfunction. We also showed that JunD was epigenetically regulated by promoter hypermethylation, post-translational modification of histone marks, and translational repression by miRNA (microRNA)-673/menin. Reduced JunD mRNA and protein expression were confirmed in left ventricular specimens obtained from patients with type 2 diabetes mellitus as compared to nondiabetic subjects. Conclusions: Here, we show that a complex epigenetic machinery involving DNA methylation, histone modifications, and microRNAs mediates hyperglycemia-induced JunD downregulation and myocardial dysfunction in experimental and human diabetes mellitus. Our results pave the way for tissue-specific therapeutic modulation of JunD to prevent diabetic cardiomyopathy.

scholarly journals Changes in the Expression of TBP-2 in Response to Histone Deacetylase Inhibitor Treatment in Human Endometrial Cells

2021 ◽  
Vol 22 (3) ◽  
pp. 1427
Author(s):  
Hye In Kim ◽  
Seok Kyo Seo ◽  
Seung Joo Chon ◽  
Ga Hee Kim ◽  
Inha Lee ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Protein Expression ◽  
Histone Deacetylase ◽  
Histone Deacetylase Inhibitors ◽  
Redox Status ◽  
Endometrial Stromal Cells ◽  
Endometrial Cells ◽  
Ros Accumulation ◽  
Ishikawa Cells ◽  
Mrna And Protein Expression

Histone deacetylase inhibitors (HDACi) induce apoptosis preferentially in cancer cells by caspase pathway activation and reactive oxygen species (ROS) accumulation. Suberoylanilide hydroxamic acid (SAHA), a HDACi, increases apoptosis via altering intracellular oxidative stress through thioredoxin (TRX) and TRX binding protein-2 (TBP-2). Because ROS accumulation, as well as the redox status determined by TBP-2 and TRX, are suggested as possible mechanisms for endometriosis, we queried whether SAHA induces apoptosis of human endometrial cells via the TRX–TBP-2 system in endometriosis. Eutopic endometrium from participants without endometriosis, and ectopic endometrium from patients with endometriosis, was obtained surgically. Human endometrial stromal cells (HESCs) and Ishikawa cells were treated with SAHA and cell proliferation was assessed using the CCK-8 assay. Real-time PCR and Western blotting were used to quantify TRX and TBP-2 mRNA and protein expression. After inducing oxidative stress, SAHA was applied. Short-interfering TRX (SiTRX) transfection was performed to see the changes after TRX inhibition. The mRNA and protein expression of TBP-2 was increased with SAHA concentrations in HESCs significantly. The mRNA TBP-2 expression was decreased after oxidative stress, upregulated by adding 2.5 μM of SAHA. The TRX/TBP-2 ratio decreased, apoptosis increased significantly, and SiTRX transfection decreased with SAHA. In conclusion, SAHA induces apoptosis by modulating the TRX/TBP-2 system, suggesting its potential as a therapeutic agent for endometriosis.

scholarly journals Tert-Butylhydroquinone Prevents Oxidative Stress-Mediated Apoptosis and Extracellular Matrix Degradation in Rat Chondrocytes

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Bo Yang ◽  
Haisheng Huang ◽  
Qisong He ◽  
Wei Lu ◽  
Lu Zheng ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Extracellular Matrix ◽  
Matrix Metalloproteinase ◽  
Protein Expression ◽  
Cell Viability ◽  
Cell Counting ◽  
Expression Levels ◽  
Extracellular Matrix Components ◽  
Mrna And Protein Expression

Oxidative stress-induced chondrocyte apoptosis and degradation of the extracellular matrix (ECM) play an important role in the progression of osteoarthritis (OA). In addition, tert-butylhydroquinone (TBHQ) is an activator of the nuclear factor erythroid derived-2-related factor 2 (Nrf2). The present study aimed to determine the effectiveness of TBHQ in preventing the apoptosis of chondrocytes and degradation of the extracellular matrix, induced by oxidative stress, in vitro. Therefore, rat chondrocytes were exposed to 20 μM tert-butyl hydroperoxide (TBHP) for 24 h to establish an oxidative damage model, in vitro. Thereafter, cell viability was evaluated using the Cell Counting Kit-8 assay. Moreover, the level of ROS was determined through 2′,7′-dichlorofluorescein diacetate staining. The mitochondrial membrane potential of chondrocytes was also measured using JC-1. Furthermore, cell apoptosis was assessed through Annexin V-fluorescein isothiocyanate/propidium iodide staining. The study also performed Western blotting and qPCR to evaluate the expression of extracellular matrix components, matrix catabolic enzymes, and changes in signalling pathways. The results showed that 2.5 and 5 μM of TBHQ reduced the TBHP-induced generation of excessive ROS and improved cell viability. Additionally, 2.5 and 5 μM of TBHQ prevented mitochondrial damage and apoptosis in rat chondrocytes. Treatment with TBHQ also increased the mRNA and protein expression levels of aggrecan and collagen II. However, TBHQ reduced the mRNA and protein expression levels of matrix metalloproteinase 3 (MMP3) and matrix metalloproteinase 13 (MMP13) in rat chondrocytes. In addition, treatment with TBHQ enhanced the protein expression levels of Nrf2, NADPH quinone oxidoreductase 1 (NQO-1), and hemeoxygenase-1 (HO-1) in rat chondrocytes. The current study showed that TBHQ was not only effective in protecting against TBHP-induced oxidative stress but also inhibited the apoptosis of rat chondrocytes and degradation of the ECM by activating the Nrf2 pathway. The results therefore suggest that TBHQ holds potential for use in the treatment of OA.

scholarly journals Nrf2 Play an Protective Role in Oxldl Induced Fibrosis in Renal Tubular Cells

2021 ◽  
Author(s):  
xiangju long ◽  
Zhe Liu ◽  
Yanan Sun ◽  
Hong Zhang
Keyword(s):  
Oxidative Stress ◽  
Protein Expression ◽  
Protein Level ◽  
Protective Role ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Nrf2 Signaling Pathway ◽  
Mrna And Protein Expression ◽  
Renal Tubular ◽  
Nrf2 Protein

Abstract CD36 is a receptor of OxLDL in kidney tubular epithelial cells(NRK-52E cells),nuclear factor erythroid 2-related factor 2 (Nrf2) is a crucial factor initiate Nrf2-signaling pathway regulating oxidative stress,kelch-like ECH-associated protein 1(Keap1) is called Nrf2 inhibitor.We treated NRK-52E cells by different concentration and time of OxLDL, and Nrf2 inhibitor ΚeapI ,and then observed CD36 ,cytoplasmic and nuleus of Nrf2 ,E-cadherinin in NRK-52E cells by western blotting and RT-PCR methods etc.,we found that CD36 protein in OxLDL stimulated NRK-52E cells increased after enough concentration and time;Although total Nrf2 protein level did not chang significantly at 5h,10h,but decreased at 24h,48h;Nuleus Nrf2 protein level increased relatively.Meanwhile, cytoplasmic Nrf2 protein level did not change significantly; CD36 mRNA and protein expression decreased in the NRK-52E renal tubular cells treated with Nrf2 inhibitor keap1; After OxLDL stimulation and then keap1 overexpression, CD36 mRNA and protein expression also decreased; E-cadherin expression decreased in NRK-52E after KeapI over-expression treatment .These results may indicateed that CD36 could accept OxLDL and then upregulated in NRK-52E cells ; Nrf2 could be activated by OxLDL, But Nrf2 could resist oxidative stress induced by OxLDL only if it transfer to the nucleus from cytoplasm.Nrf2 may play an protective role through upregulating CD36 .

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