scholarly journals MG132 Ameliorates Kidney Lesions by Inhibiting the Degradation of Smad7 in Streptozotocin-Induced Diabetic Nephropathy

2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Chenlin Gao ◽  
Keri Aqie ◽  
Jianhua Zhu ◽  
Guo Chen ◽  
Ling Xu ◽  
...  
Keyword(s):  
Diabetic Nephropathy ◽  
Protein Expression ◽  
Transforming Growth Factor ◽  
Regulatory Protein ◽  
Kidney Damage ◽  
The Body ◽  
Control Group ◽  
Kidney Weight ◽  
Diabetes Group ◽  
Ubiquitin Proteasome

Background. Smad7 is the main negative regulatory protein in the transforming growth factor-β(TGF-β) downstream signaling pathway, which plays an important role in diabetic nephropathy (DN) and may be related to the ubiquitin proteasome pathway (UPP).Aim. We investigated the role of UPP in regulating TGF-β/SMAD signaling and explored the therapeutic effect of the ubiquitin proteasome inhibitor MG132 on DN.Methods. Wistar rats were randomly divided into a diabetes group and a normal control group. Rats in the diabetes group were injected intraperitoneally with streptozotocin. Diabetic rats were then randomly divided into a diabetic nephropathy group (DN group), an MG132 high concentration (MH) group, and an MG132 low concentration (ML) group. After 8 weeks of treatment, 24-hour urinary microalbumin (UAlb), urinary protein/urinary creatinine (Up/Ucr) values, ALT, AST, Bcr, kidney damage, TGF-β, Smad7, fibronectin (FN), and Smurf2 were detected.Results. The body mass and Smad7 protein expression decreased in DN group, but kidney weight, kidney weight index, UAlb, Up/Ucr, FN and Smurf2 mRNA expression, and TGF-βprotein expression increased. However, these changes diminished following treatment with MG132, and a more pronounced effect was evident in MH group compared to ML group.Conclusion. MG132 alleviates kidney damage by inhibiting Smad7 ubiquitin degradation and TGF-βactivation in DN.

scholarly journals The Proteasome Inhibitor, MG132, Attenuates Diabetic Nephropathy by Inhibiting SnoN DegradationIn VivoandIn Vitro

2014 ◽  
Vol 2014 ◽  
pp. 1-11 ◽  
Author(s):  
Wei Huang ◽  
Chen Yang ◽  
Qinling Nan ◽  
Chenlin Gao ◽  
Hong Feng ◽  
...  
Keyword(s):  
Diabetic Nephropathy ◽  
High Glucose ◽  
Proteasome Inhibitor ◽  
Kidney Damage ◽  
Control Group ◽  
Glomerular Mesangial Cells ◽  
Proteasome Inhibitor Mg132 ◽  
Ubiquitin Proteasome Pathway ◽  
Ubiquitin Proteasome ◽  
Proteasome Pathway

Transforming growth factor-β(TGF-β) has been shown to be involved in diabetic nephropathy (DN). The SnoN protein can regulate TGF-βsignaling through interaction with Smad proteins. Recent studies have shown that SnoN is mainly degraded by the ubiquitin-proteasome pathway. However, the role of SnoN in the regulation of TGF-β/Smad signaling in DN is still unclear. In this study, diabetic rats were randomly divided into a diabetic control group (DC group) and a proteasome inhibitor (MG132) diabetes therapy group (DT group). Kidney damage parameters and the expression of SnoN, Smurf2, and TGF-βwere observed. Simultaneously, we cultured rat glomerular mesangial cells (GMCs) stimulated with high glucose, and SnoN and Arkadia expression were measured. Results demonstrated that 24-hour urine protein, ACR, BUN, and the expression of Smurf2 and TGF-βwere significantly increased (P<0.05), whereas SnoN was significantly decreased in the DC group (P<0.05). However, these changes diminished after treatment with MG132. SnoN expression in GMCs decreased significantly (P<0.05), but Arkadia expression gradually increased due to high glucose stimulation (P<0.05), which could be almost completely reversed by MG132 (P<0.05). The present results support the hypothesis that MG132 may alleviate kidney damage by inhibiting SnoN degradation and TGF-βactivation, suggesting that the ubiquitin-proteasome pathway may become a new therapeutic target for DN.

scholarly journals Assessment of serum Ferritin level and its correlation with HbA1c in Diabetic Nephropathy

2020 ◽  
Vol 11 (2) ◽  
pp. 46-51
Author(s):  
Madhura Navule Siddappa ◽  
Kowsalya Ramprasad
Keyword(s):  
Diabetic Nephropathy ◽  
Glycemic Control ◽  
Serum Ferritin ◽  
Serum Ferritin Level ◽  
Ferritin Level ◽  
Pearson Correlation ◽  
The Body ◽  
Control Group ◽  
Type Ii

Background: Serum ferritin levels reflecting the body iron stores, is known to be elevated in type 2 Diabetes Mellitus. However its association with diabetic complications including Diabetic nephropathy (DN), and overall glycemic control needs to be validated. Aims and Objectives: The aim of this study was to find the Serum Ferritin level abnormalities in DM patients with nephropathy in comparison with DM patients without nephropathy and to find correlation of Serum Ferritin (SF) levels with levels of Glycated Hemoglobin (HbA1c) in patients with diabetic nephropathy. Materials and Methods: This is a retrospective study, which included eighty five registered patients with Type 2 DM (44 Type II DM without nephropathy cases and 41 cases of Type II DM with nephropathy). SF and HbA1c was estimated in all cases across both the groups and were compared with age and sex matched controls and analysed. Results: Serum Ferritin levels were higher in diabetics with nephropathy compared to diabetics without nephropathy (p<0.0001). SF levels were higher in diabetic groups compared to control group (p <0.001).The correlation between HbA1c and SF was assessed among all cases of DM with nephropathy group using pearson correlation test and it showed a significantly positive correlation (r=0.431) with a SF (mean = 938±148) and HbA1c (mean = 9.2±2.02). Conclusion: Serum ferritin levels positively correlate with HbA1c levels in Type II DM cases with nephropathy, which suggests that serum Ferritin levels can be used as a surrogate marker of glycemic control in Type II DM with nephropathy.

scholarly journals DIABETIC NEPHROPATHY

2018 ◽  
Vol 25 (07) ◽  
pp. 1117-1123
Author(s):  
Faiza Irshad ◽  
Rabia Sajjad Toor ◽  
Madiha Hussain
Keyword(s):  
Body Weight ◽  
Diabetic Nephropathy ◽  
Serum Creatinine ◽  
Aqueous Extract ◽  
Antioxidant Properties ◽  
Control Group ◽  
Albino Rats ◽  
P Value ◽  
Kidney Weight ◽  
Experimental Group

Background: Zingiber Officinale Roscoe (Zingiberaceae family) is knownas Ginger. It is famous for its antioxidant properties. Objectives: To evaluate the effects ofGinger aqueous extract on the serum creatinine and paired kidney weight in Alloxan induceddiabetic nephropathy of albino rats. Study Design: Experimental study. Period: 06 months01-01-2013 to 30 June 2013. Setting: Anatomy Department, Sheikh Zayed, PGMI Lahore.Materials and Methods: Diabetes mellitus was induced with Alloxan intraperitoneally (150 mg/kg body weight) in Experimental groups B & C. Then the rats of experimental group C received200mg/kg body weight of ginger aqueous extract by gavage daily for five weeks starting from8th day after Alloxan injection. Results: Serum creatinine levels increased more in experimentalgroup B as compared to experimental group C. Group wise comparison of creatinine levelrevealed that the difference among control (A group) and experimental (B & C Groups) wassignificant having p-value <0.001. We observed that Paired kidney weight in experimentalgroup B increased as compared to control group A. Less increase in the paired kidney weightwas observed in experimental group C as compared to experimental group B. The differenceof mean paired kidney weight among three groups was significant having p-value <0.001.Conclusion: The results of the present study indicated that the co-treatment of Ginger aqueousextract prevented alloxan induced diabetic nephropathy in albino rats. The aqueous extract ofGinger showed amazing results on paired kidney weight.

scholarly journals Yiqi Huoxue Recipe Regulates Autophagy through Degradation of Advanced Glycation End Products via mTOR/S6K1/LC3 Pathway in Diabetic Nephropathy

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Liang Chen ◽  
Linghao Dai ◽  
Yi Liu ◽  
Xinyue Li ◽  
Hui Wang
Keyword(s):  
Body Weight ◽  
Diabetic Nephropathy ◽  
Advanced Glycation End Products ◽  
Periodic Acid ◽  
The Body ◽  
Advanced Glycation ◽  
Kidney Weight ◽  
Expression Levels ◽  
Glycation End Products ◽  
End Products

Background. Yiqi Huoxue recipe can delay the progression of diabetic nephropathy, but its treatment mechanism is still unclear. We aimed to explore the effects of Yiqi Huoxue recipe on autophagy in diabetic nephropathy and its underlying mechanism. Methods. All rats were randomly divided into seven groups. The body weight, kidney weight, blood glucose, glycated hemoglobin, urine protein, urine microprotein, creatinine, urea nitrogen, triglyceride, and lipoprotein were analyzed. HE, Masson, and periodic acid-Schiff staining were used to detect the severity of pathological changes in kidneys. The level of advanced glycation end products was assessed by the ELISA. Immunofluorescence staining was performed to check the expressions of podocin and nephrin. The expression levels of mTOR/S6K1/LC3 pathway-related proteins and mRNA were detected by qRT-PCR and western blotting. Results. Yiqi Huoxue recipe significantly elevated body weight and significantly decreased kidney weight and kidney index. Yiqi Huoxue recipe significantly affected the levels of biochemical indicators in diabetic nephropathy and showed a regulatory effect on kidney damage and lipid metabolism disorders. ELISA showed that Yiqi Huoxue recipe significantly reduced the level of advanced glycation end products. The expressions of nephrin and podocin increased significantly, depending on the dosage of Yiqi Huoxue recipe. Additionally, Yiqi Huoxue recipe regulated the expression levels of p-AKT, mTOR, S6K1, and LC3. Conclusion. Yiqi Huoxue recipe regulates podocyte autophagy to promote the degradation of advanced glycation end products through mTOR/S6K1/LC3 pathway. It has a certain guiding significance for the diagnosis and treatment of diabetic nephropathy.

scholarly journals Lovastatin Inhibits Transforming Growth Factor-β1 Expression in Diabetic Rat Glomeruli and Cultured Rat Mesangial Cells

2000 ◽  
Vol 11 (1) ◽  
pp. 80-87
Author(s):  
SUNG IL KIM ◽  
DONG CHEOL HAN ◽  
HI BAHL LEE
Keyword(s):  
Diabetic Nephropathy ◽  
Blood Glucose ◽  
Transforming Growth Factor ◽  
Mesangial Cells ◽  
Diabetic Rats ◽  
Kidney Weight ◽  
Urine Albumin Excretion ◽  
Urine Albumin ◽  
Ecm Proteins ◽  
Tgf Β1

Abstract. Diabetic nephropathy is a leading cause of end-stage renal disease and is characterized by excessive deposition of extracellular matrix (ECM) proteins in the glomeruli. Transforming growth factor-β (TGF-β) is the major mediator of excessive accumulation of ECM proteins in diabetic nephropathy through upregulation of genes encoding ECM proteins as well as downregulation of genes for ECM-degrading enzymes. It has been shown that lovastatin, an inhibitor of 3-hydroxy-3-methylglutaryl CoA reductase, delays the onset and progression of different models of experimental nephropathy. To evaluate the effect of lovastatin on the development and progression of diabetic nephropathy, streptozotocin-induced diabetic rats were studied for 12 mo. In untreated diabetic rats, there were significant increases in blood glucose, urine albumin excretion, kidney weight, glomerular volume, and TGF-β1 mRNA expression in the glomeruli compared with normal control rats treated with citrate buffer only. Treatment with lovastatin in diabetic rats significantly suppressed the increase in urine albumin excretion, kidney weight, glomerular volume, and TGF-β1 mRNA expression despite high blood glucose levels. To elucidate the mechanisms of the renal effects of lovastatin, rat mesangial cells were cultured under control (5.5 mM) or high (30 mM) glucose with lovastatin alone, mevalonate alone, or with both. Under high glucose, TGF-β1 and fibronectin mRNA and proteins were upregulated. These high glucose-induced changes were suppressed by lovastatin (10 μM) and nearly completely restored by mevalonate (100 μM). These results suggest that lovastatin has a direct cellular effect independent of a cholesterol-lowering effect and delays the onset and progression of diabetic nephropathy, at least in part, through suppression of glomerular expression of TGF-β1.

scholarly journals Effects of resveratrol on changes induced by high-fat feeding on clock genes in rats

2013 ◽  
Vol 110 (8) ◽  
pp. 1421-1428 ◽  
Author(s):  
Jonatan Miranda ◽  
María P. Portillo ◽  
Juan Antonio Madrid ◽  
Noemí Arias ◽  
M. Terasa Macarulla ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Protein Expression ◽  
Fatty Acid Synthase ◽  
Clock Genes ◽  
The Body ◽  
Control Group ◽  
Standard Diet ◽  
High Fat ◽  
Peripheral Tissues ◽  
Fat Feeding

In mammals, the main component of the circadian system is the suprachiasmatic nucleus in the hypothalamus. However, circadian clocks are also present in most peripheral tissues, such as adipose tissue. The aim of the present study was to analyse the potential effects of resveratrol on changes induced by high-fat feeding in the expression of clock genes and clock-controlled genes in the white adipose tissue from rats. For this purpose, rats were divided into three groups: a control group, fed a standard diet, and two other groups, either fed a high-fat diet supplemented with resveratrol (RSV) or no resveratrol (HF). The expression of clock genes and clock-controlled genes was analysed by RT-PCR. Protein expression and fatty acid synthase (FAS) activity were also analysed. When comparing the controls, the RSV group showed similar patterns of response to the HF group, except for reverse erythroblastosis virus α (Rev-Erbα), which was down-regulated. The expression of this gene reached the same levels as in control rats. The response pattern of protein expression forRev-Erbαwas similar to that found for gene expression. High-fat feeding up-regulated all adipogenic genes and resveratrol did not modify them. In the HF group, the activity of FAS tended to increase, while resveratrol decreased. In conclusion, resveratrol reverses the change induced by high-fat feeding in the expression ofRev-Erbαin adipose tissue, which means that clock machinery is a target for this polyphenol. This change seems to be related to reduced lipogenesis, which might be involved in the body fat-lowering effect of this molecule.

scholarly journals Nephroprotective Effect of POLYCAN on Acute Renal Failure Induced by Cisplatin in Rats

2012 ◽  
Vol 2012 ◽  
pp. 1-6 ◽  
Author(s):  
Sae-Kwang Ku ◽  
Young-Joon Lee ◽  
Sung-Dong Lee ◽  
Hyung-Rae Cho ◽  
Seung-Bae Moon ◽  
...  
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Creatinine Level ◽  
Vehicle Control ◽  
The Body ◽  
Control Group ◽  
Kidney Weight ◽  
Vehicle Control Group ◽  
Sham Control Group ◽  
Nephroprotective Effect

We performed to evaluate the effect of POLYCAN (β-glucan) on cisplatin-(CDDP-)induced acute renal failure (ARF) in rats. POLYCAN was administered orally once a day for 32 days. Each of 8 rats per group was selected based on the body weight (BW) after acclimatization and they were sacrificed at 5 days after CDDP injection. There was significant (P<0.05) increase of BW after CDDP dosing in all POLYCAN groups than vehicle control and significant (P<0.01 or P<0.05) decrease of absolute and relative kidney weight were detected in all POLYCAN groups compared with vehicle control. In addition, serum BUN and creatinine level in all POLYCAN groups were significantly (P<0.01 or P<0.05) lower than vehicle control and the percentage of degenerative regions significantly (P<0.01) decreased in all POLYCAN groups. As the results of CDDP-induced ARF process, dramatic decrease of the BW, increase of the kidney weight, serum BUN, and creatinine level were detected in vehicle control group compared with sham control group. The changes by CDDP-induced ARF process in POLYCAN groups were significantly and dose-dependently improved compared with vehicle control group. Therefore, POLYCAN has enough potential to develop as a new agent of prevention or treatment for ARF.

scholarly journals The Favored Mechanism for Coping with Acute Cold Stress: Upregulation of miR-210 in Rats

2018 ◽  
Vol 46 (5) ◽  
pp. 2090-2102 ◽  
Author(s):  
Wenjin Guo ◽  
Shuai Lian ◽  
Li Zhen ◽  
Shucheng Zang ◽  
Yan Chen ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Death ◽  
Relative Humidity ◽  
Protein Expression ◽  
Cold Stress ◽  
The Body ◽  
Control Group ◽  
Qrt Pcr ◽  
Extracellular Flux ◽  
Glucose Flux

Background/Aims: The main aim of this study was to determine the mechanisms by which rno-miR-210-3p affects changes in gene expression, metabolism, apoptosis and proliferation of cells under acute cold stress (ACS) conditions. Methods: The treatment group (n=6, weight 340±20 g) was exposed to ACS (temperature 4±0.5°C, relative humidity 45±0.5%) and the control group (n=6, weight 340±20 g) to normal temperature (NT) (temperature 24±0.5°C, relative humidity 45±0.5%). Rat liver samples were collected for qRT-PCR and western blot analyses to detect relative expression of rno-miR-210-3p, ISCU, Rap1b, ATP1b1, GPD1, E2F3, RAD52, PSMB6 and GPD2. For cell experiments, 100 pmol/dish rno-miR-210-3p mimic and 150 pmol/dish rno-miR-210-3p inhibitor were used. Mitochondrial glucose flux and glycolysis were measured using the XFe24 Extracellular Flux Analyzer. Cells were collected for apoptosis analysis 24 h after transfection and proliferation was quantified using the WST-1 Cell Proliferation and Cytotoxicity Assay Kit (Beyotime, Shanghai, China), according to the manufacturerʹs instructions. Results: In the rat experiment, expression of rno-miR-210-3p under ACS was increased sharply while ISCU, E2F3, RAD52, and PSMB6 levels declined, along with protein expression of ISCU and PSMB6. In cell experiments, ISCU, Rap1b, ATP1b1, GPD1, E2F3, RAD52, PSMB6 and GPD2 genes were downregulated while ISCU and PSMB6 protein expression decreased with upregulation of rno-miR-210-3p. Conversely, in response to decreased rno-miR-210-3p expression, ISCU, E2F3, RAD52, PSMB6 and GPD2 genes were upregulated, in addition to ISCU and PSMB6 proteins. Upregulation of miR-210 inhibited cell proliferation and induced cell death whereas its downregulation promoted cell proliferation. Upregulation or downregulation of miR-210 promoted glycolysis and mitochondrial respiration of BRL cells. However, downregulation of miR-210 caused acid production in cells. Conclusion: Expression of rno-miR-210-3p is significantly increased under ACS. Upregulation of rno-miR-210-3p inhibits the expression of ISCU, Rap1b, ATP1b1, GPD1, E2F3, RAD52, PSMB6 and GPD2 genes, promotes glycolysis of liver and enhances the mitochondrial respiratory capacity of cells, but may also cause cell death. Our findings collectively indicate that regulation of rno-miR-210-3p is a preferential mechanism of choice used by the body to cope with ACS.

scholarly journals Evaluation of kidney injury molecule-1 as a disease progression biomarker in diabetic nephropathy

2019 ◽  
Vol 35 (4) ◽  
Author(s):  
Fatima Abid Khan ◽  
Syeda Sadia Fatima ◽  
Ghulam Mustafa Khan ◽  
Sana Shahid
Keyword(s):  
Diabetic Nephropathy ◽  
Disease Progression ◽  
Kidney Function ◽  
Kidney Injury ◽  
Positive Association ◽  
Kidney Damage ◽  
Control Group ◽  
Diabetic Patients ◽  
Kidney Injury Molecule 1

Background & Objective: Kidney Injury Molecule-1 (KIM-1) is a peptide whose release into circulation is specific to tubular injury. This study aimed to estimate levels of kidney injury molecule-1 in diabetic patients with and without kidney disease. And evaluate the role of KIM-1 as an early screening marker of progressive kidney injury. Methods: This follow-up study included n=85 subjects from the diabetic clinic of Jinnah Post Graduate Medical Center (JPMC) in collaboration with Aga Khan University from November 2016 till September 2017 They were divided as: i) Group A1 (n=30) participants with diabetes for <5 years without microalbuminuria ii) Group A2 (n= 30) subjects with diabetes for 6-10 years with microalbuminuria; iii) Group B (n=25) subjects as healthy control group. All study participants were followed for 6 months and their blood glucose, urea, creatinine, electrolytes, albuminuria and serum KIM-1 were assayed. Results: High KIM-1 at baseline was present in group A2 patients as compared to controls and group A1 (p<0.001). Higher levels were seen after six months in group A1 along with the presence of micro albuminuria (p<0.001) suggesting kidney damage. Moderate positive association were seen for KIM1 with creatinine levels (r=0.530; p<0.001), and HbA1c (r=0.576; p<0.001) in all patients. While a strong positive association was seen for blood urea nitrogen as a marker for kidney function both at baseline (r= 0.728; p=0.000) and follow up (r=0.747; p=0.001). Multiple logistic regression controlling for age showed that KIM1 was independently associated with BUN (r=0.727; p<0.001), creatinine (r=0.510; p<0.001) and HbA1c (r=0.401; p=0.008) in all groups. Conclusion: Rising KIM-1 levels with progressive kidney damage with or without derangement of kidney function is reported in this study. This finding may pave a way towards identifying KIM1 as a prognostic marker for kidney injury. doi: https://doi.org/10.12669/pjms.35.4.154 How to cite this:Khan FA, Fatima SS, Khan GM, Shahid S. Evaluation of kidney injury molecule-1 as a disease progression biomarker in diabetic nephropathy. Pak J Med Sci. 2019;35(4):---------. doi: https://doi.org/10.12669/pjms.35.4.154 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

scholarly journals 5-aminoisoquinoline improves renal function and fibrosis during recovery phase of cisplatin-induced acute kidney injury in rats

2018 ◽  
Vol 38 (2) ◽  
Author(s):  
Andrés Quesada ◽  
Francisco O’Valle ◽  
Sebastián Montoro-Molina ◽  
Mercedes Gómez-Morales ◽  
Mercedes Caba-Molina ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Body Weight ◽  
Renal Dysfunction ◽  
Transforming Growth Factor ◽  
Smooth Muscle Actin ◽  
Kidney Injury ◽  
Body Weight Loss ◽  
Recovery Phase ◽  
The Body ◽  
Control Group

The aim of the present study is to analyze the effects of 5-aminoisoquinoline (5-AIQ), a poly(ADP-ribose) polymerase-1 (PARP1) inhibitor, over renal dysfunction and fibrosis during recovery phase of cisplatin (CisPt)-induced acute kidney injury (AKI) in rats. Male Wistar rats were distributed in three groups (n=8 each group): control, CisPt, and CisPt + 5-AIQ. Control and CisPt groups received a subcutaneous injection of either saline or 7 mg/kg CisPt, respectively. CisPt + 5-AIQ group received two intraperitoneal injections of 10 mg/kg 5-AIQ 2 h before and 24 h after CisPt treatment. Thirteen days after the treatment, rats were housed in metabolic cages and 24-h urine collection was made. At day 14, CisPt-treated rats showed increased diuresis, N-acetyl-β-d-glucosaminidase (NAG) excretion, glucosuria and sodium fractional excretion (NaFE), and decreased creatinine clearance (CrCl). 5-AIQ significantly increased CrCl and decreased NAG excretion, glucosuria, and NaFE. In plasma, CisPt increased sodium, urea, and creatinine concentrations, while 5-AIQ treatment decreased these variables to the levels of control group. 5-AIQ completely prevented the body weight loss evoked by CisPt treatment. CisPt also induced an increased renal expression of PAR polymer, α-smooth muscle actin (α-SMA), transforming growth factor-β1 (TGF-β1), and collagen-IV. These variables were decreased in CisPt + 5-AIQ group. Tubular lesions and renal fibrosis were also decreased by 5-AIQ treatment. We conclude that inhibition of PARP1 with 5-AIQ can attenuate long-term nephrotoxic effects associated with the CisPt treatment, preventing renal dysfunction and body weight decrease and ameliorating tubular lesions and collagen deposition.

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