scholarly journals Alpha-Lipoic Acid Attenuates Renal Injury in Rats with Obstructive Nephropathy

2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Orawan Wongmekiat ◽  
Dolrawee Leelarungrayub ◽  
Kamthorn Thamprasert
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Lipoic Acid ◽  
Renal Injury ◽  
Ureteral Obstruction ◽  
Structural Changes ◽  
Transforming Growth Factor ◽  
Interstitial Fibrosis ◽  
Obstructive Nephropathy ◽  
Alpha Lipoic Acid

This study was established to determine the possible protective effects of alpha-lipoic acid (ALA), a powerful antioxidant, on renal injury in obstructive nephropathy. Male Sprague-Dawley rats were assigned into sham-operated unilateral ureteral obstruction (UUO) and UUO treated with ALA groups. ALA 60 mg/kg was injected intraperitoneally 2 days before UUO induction and continued afterward for 7 days. Renal function, oxidative stress markers, nitric oxide, transforming growth factor-1 (TGF-β1), and histological changes were evaluated at the end of the experiment. Obstruction of the ureter resulted in renal dysfunction as indicated by significant increases in blood urea nitrogen and serum creatinine. Nonobstructed contralateral kidneys in all groups examined did not show any morphological or biochemical alterations. In untreated UUO group, the obstructed kidney developed marked hydronephrosis, leukocyte infiltration, and severe interstitial fibrosis. These functional and structural changes were associated with significant increases in tissue levels of malondialdehyde, nitric oxide, and TGF-β1 but decreases in reduced glutathione and total antioxidant capacity. Pretreatment with ALA significantly minimized all the changes elicited by ureteral obstruction. These findings demonstrate that ALA supplementation attenuates renal injury in rats with obstructive nephropathy and further suggest that oxidative stress inhibition is likely to be involved in the beneficial effects of this compound.

Influence of alpha-lipoic acid on nicotine-induced lung and liver damage in experimental rats

2017 ◽  
Vol 95 (5) ◽  
pp. 492-500 ◽  
Author(s):  
Hayam Ateyya ◽  
Manar A. Nader ◽  
Ghalia M. Attia ◽  
Nagla A. El-Sherbeeny
Keyword(s):  
Oxidative Stress ◽  
Liver Damage ◽  
Lipoic Acid ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Liver Enzymes ◽  
Histopathological Examination ◽  
Alpha Lipoic Acid ◽  
Defensive Role ◽  
Tgf Β1

Nicotine mediates some of the injurious effects caused by consuming tobacco products. This work aimed at investigating the defensive role of alpha-lipoic acid (ALA) with its known antioxidant and antiinflammatory effect in nicotine-induced lung and liver damage. Rats were arranged into 4 groups: control, nicotine, ALA, and ALA–nicotine groups. Oxidative stress and antioxidant status were determined by assessing thiobarbituric acid reactive substances (TBARS), superoxide dismutase (SOD), and glutathione (GSH) levels in lung and liver. Liver enzymes and lipid profiles were measured and pulmonary and hepatic damage were assessed by histopathological examination. Also, serum levels of transforming growth factor beta 1 (TGF-β1) and vascular cell adhesion molecule 1 (VCAM-1) were determined. The results revealed an increase in TBARS in tissues and a reduction in both SOD and GSH activity in the nicotine-treated rats. Nicotine induced high levels of liver enzymes, TGF-β1, VCAM-1, and dyslipidemia with histopathological changes in the lung and liver. ALA administration along with nicotine attenuated oxidative stress and normalized the SOD and GSH levels, ameliorated dyslipidemia, and improved TGF-β1 and VCAM-1 with better histopathology of the lung and liver. The study data revealed that ALA may be beneficial in alleviating nicotine-induced oxidative stress, dyslipidemia, and both lung and liver damage.

Gene expression reveals vulnerability to oxidative stress and interstitial fibrosis of renal outer medulla to nonhypertensive elevations of ANG II

2003 ◽  
Vol 284 (5) ◽  
pp. R1219-R1230 ◽  
Author(s):  
Baozhi Yuan ◽  
Mingyu Liang ◽  
Zhizhang Yang ◽  
Elizabeth Rute ◽  
Norman Taylor ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Western Blot ◽  
Renal Injury ◽  
Interstitial Fibrosis ◽  
Control Period ◽  
Renal Medulla ◽  
Differentially Expressed ◽  
Ang Ii ◽  
Outer Medulla ◽  
Renal Outer Medulla

The present study was designed to determine whether nonhypertensive elevations of plasma ANG II would modify the expression of genes involved in renal injury that could influence oxidative stress and extracellular matrix formation in the renal medulla using microarray, Northern, and Western blot techniques. Sprague-Dawley rats were infused intravenously with either ANG II (5 ng · kg−1 · min−1) or vehicle for 7 days ( n = 6/group). Mean arterial pressure averaged 110 ± 0.6 mmHg during the control period and 113 ± 0.4 mmHg after ANG II. The mRNA of 1,751 genes (∼80% of all currently known rat genes) that was differentially expressed (ANG II vs. saline) in renal outer and inner medulla was determined. The results of 12 hybridizations indicated that in response to ANG II, 11 genes were upregulated and 25 were downregulated in the outer medulla, while 11 were upregulated and 13 were downregulated in the inner medulla. These differentially expressed genes, most of which were not known previously to be affected by ANG II in the renal medulla, were found to group into eight physiological pathways known to influence renal injury and kidney function. Particularly, expression of several genes would be expected to increase oxidative stress and interstitial fibrosis in the outer medulla. Western blot analyses confirmed increased expression of transforming growth factor-β1 and collagen type IV proteins in the outer medulla. Results demonstrate that nonhypertensive elevations of plasma ANG II can significantly alter the expression of a variety of genes in the renal outer medulla and suggested the vulnerability of the renal outer medulla to the injurious effect of ANG II.

Alpha-lipoic acid and coenzyme Q10 combination ameliorates experimental diabetic neuropathy by modulating oxidative stress and apoptosis

Life Sciences ◽  
2019 ◽  
Vol 216 ◽  
pp. 101-110 ◽  
Author(s):  
Nasrin Sadeghiyan Galeshkalami ◽  
Mohammad Abdollahi ◽  
Rezvan Najafi ◽  
Maryam Baeeri ◽  
Akram Jamshidzade ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Diabetic Neuropathy ◽  
Lipoic Acid ◽  
Coenzyme Q10 ◽  
Alpha Lipoic Acid ◽  
Experimental Diabetic Neuropathy

Alpha-lipoic acid defends homocysteine-induced endoplasmic reticulum and oxidative stress in HAECs

2016 ◽  
Vol 80 ◽  
pp. 63-72 ◽  
Author(s):  
Huimin Hu ◽  
Changyuan Wang ◽  
Yue Jin ◽  
Qiang Meng ◽  
Qi Liu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endoplasmic Reticulum ◽  
Lipoic Acid ◽  
Alpha Lipoic Acid ◽  
And Oxidative Stress

scholarly journals The role of oxidative stress and effect of alpha-lipoic acid in reexpansion pulmonary edema – an experimental study

2010 ◽  
Vol 6 ◽  
pp. 848-853 ◽  
Author(s):  
Seyfettin Gumus ◽  
Orhan Yucel ◽  
Mehmet Gamsizkan ◽  
Ayse Eken ◽  
Omer Deniz ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Experimental Study ◽  
Pulmonary Edema ◽  
Lipoic Acid ◽  
Alpha Lipoic Acid ◽  
Reexpansion Pulmonary Edema

scholarly journals Alpha-Lipoic Acid Protects Rat Kidney Against Oxidative Stress-Mediated DNA Damage and Apoptosis Induced by Lead

2015 ◽  
Vol 6 (1) ◽  
pp. 1-14 ◽  
Author(s):  
Samy Ali Hussein ◽  
Mohamed Ragaa R. Hassanein ◽  
Aziza Amin ◽  
Asmaa H. Mohammad Hussein
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Lipoic Acid ◽  
Rat Kidney ◽  
Alpha Lipoic Acid

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

Renal Failure ◽  
2012 ◽  
Vol 34 (7) ◽  
pp. 907-914 ◽  
Author(s):  
Xiaofang Yu ◽  
Hong Liu ◽  
Jianzhou Zou ◽  
Jiaming Zhu ◽  
Xunhui Xu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipoic Acid ◽  
Rat Model ◽  
Alpha Lipoic Acid

scholarly journals Bone Morphogenetic Protein-2 Antagonizes Renal Interstitial Fibrosis by Promoting Catabolism of Type I Transforming Growth Factor-β Receptors

Endocrinology ◽  
2009 ◽  
Vol 150 (2) ◽  
pp. 727-740 ◽  
Author(s):  
Yu-Lin Yang ◽  
Yi-Shiuan Liu ◽  
Lea-Yea Chuang ◽  
Jinn-Yuh Guh ◽  
Tao-Chen Lee ◽  
...  
Keyword(s):  
Bone Morphogenetic Protein ◽  
Ureteral Obstruction ◽  
Time Course ◽  
Transforming Growth Factor ◽  
Interstitial Fibrosis ◽  
Unilateral Ureteral Obstruction ◽  
Bone Morphogenetic Protein 2 ◽  
Type I ◽  
Morphogenetic Protein ◽  
Tgf Β1

TGF-β is a therapeutic target for renal fibrosis. Scientists have long sought ways to antagonize TGF-β to ameliorate diabetic nephropathy. Bone morphogenetic protein (BMP-2) is a member of the TGF-β superfamily and is highly regulated in the kidney. Thus, the role of BMP-2 was investigated in NRK-49F cells (rat fibroblasts). We showed that TGF-β1 induces an increase in fibronectin. Treatment with exogenous BMP-2 or pCMV-BMP-2 significantly reversed the TGF-β1-induced increase in fibronectin concomitant with a significant decrease in type I TGF-β receptors (TGF-β RI). Moreover, BMP-2 significantly shortened the half-life of TGF-β RI. These results are related to proteosomal activation because MG132, a proteasome inhibitor, abolished BMP-2-mediated degradation of TGF-β RI. This was confirmed because BMP-2 time course dependently enhanced the ubiquitination level of TGF-β RI. In addition, Smads would seem to be involved in the interaction of BMP-2 and TGF-β. We demonstrated that BMP-2 significantly reversed the TGF-β1-induced increase in pSmad2/3 and reversed the TGF-β1-induced decrease in inhibitory Smad7. Most importantly, Smad7 small interfering RNA abolished the BMP-2-induced decrease in TGF-β RI. We evaluated the clinical efficacy of BMP-2 using unilateral ureteral obstruction rats. BMP-2 was administered ip for 7 d. In the unilateral ureteral obstruction kidneys, interstitial fibrosis was prominent. However, treatment with BMP-2 dramatically reduced Masson’s trichrome staining (collagen) in the interstitial and tubular areas of the kidneys concomitantly with a reduction in TGF-β RI. These results suggest that BMP-2 acts as a novel fibrosis antagonizing cytokine partly by down-regulating TGF-β RI and Smads. Bone morphogenetic protein-2 can antagonize TGF-β-inducing cellular fibrosis by intervening post-receptors signaling, thus disclosing an application of therapeutical potential against fibrosis disorders.

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