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Submitted: 02 Feb 2019
Accepted: 30 May 2019
ePublished: 14 Jul 2019
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Immunopathol Persa. 2019;5(2): e19.
doi: 10.15171/ipp.2019.19

Scopus ID: 85147096927
  Abstract View: 2985
  PDF Download: 1615

Original

Antioxidative and anti-inflammatory impact of valsartan against renal ischemia-reperfusion injury; role of nitric oxide signaling pathway

Leila Mohmoodnia 1 ORCID logo, Sarina Safari Ahmadvand 2, Sahar Koushki 2, Behrooz Farzan 3 ORCID logo, Sajad Papi 4, Babak Hadian 5 ORCID logo, Ahmad-Reza Dehpour 6,7 ORCID logo, Amin Hasanvand 8* ORCID logo

1 Cancer Research Center, Shahrekord University of Medical Sciences, Shahrekord, Iran
2 Student Research Committee, Lorestan University of Medical Sciences, Khorramabad, Iran
3 Faculty of Medicine, Lorestan University of Medical Sciences, Khorramabad, Iran
4 Razi Herbal Medicines Research Center, Lorestan University of Medical Sciences, Khorramabad, Iran
5 Department of Internal Medicine, Lorestan University of Medical Sciences, Khorramabad, Iran
6 Experimental Medicine Research Center, Tehran University of Medical Sciences, Tehran, Iran
7 Department of Pharmacology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
8 Hepatitis Research Center, Department of Pharmacology and Toxicology, Faculty of Pharmacy, Lorestan University of Medical Sciences, Khorramabad, Iran
*Corresponding Author: *Correspondence to Amin Hasanvand, Ph.D., Email: , Email: Amin.Hasanvand@lums.ac.ir

Abstract

Introduction: Renal ischemia reperfusion injury is one of the main causes of acute renal failure, which is associated with high mortality. Tissue damage caused by ischemia-reperfusion occurs due to the release of oxygen free radicals. Type I angiotensin receptor antagonists such as valsartan can be useful in the treatment of chronic kidney disease and hypertension.

Objectives: We aimed to evaluate the protective effect of valsartan against renal ischemia reperfusion via antioxidant property and nitric oxide (NO) signaling pathway.

Materials and Methods: Fifty male Wistar rats (220±10 g) were randomly divided into five groups as follows: Group 1; healthy rats without ischemia-reperfusion (control group). Group 2; rats with ischemia reperfusion (IR) (IR control group). Group 3; rats with IR which received 30 mg/kg valsartan orally. Group 4; rats with IR which received 30 mg/kg valsartan together with 40 mg/kg L-NAME. Group 5; rats with IR which received 30 mg/kg valsartan together with 40 mg/kg L-arginine. To induce ischemia-reperfusion, rats were anesthetized with thiopental and underwent surgery. Then, we induced ischemia with blocking blood vessels for 45 minutes by clamping. Biochemical parameters including urea and creatinine were measured using commercial kits. Oxidative stress and inflammatory parameters were measured by ELISA method. Renal tissues were stained with hematoxylin and eosin. Finally, the Kolmogorov-Smirnov test was used to determine the normal distribution of data.

Results: The findings of this study indicated that treatment with valsartan and valsartan plus L-arginine leads to significant decrease in the serum levels of creatinine, urea, and albumin/creatinine, malondialdehyde (MDA), interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) in contrast to IR control group which has increased level of these parameters. On the other hand, treatment with valsartan and valsartan plus L-arginine lead to increase in the serum levels of glutathione peroxidase (GPX), in contrast to ischemia reperfusion control group.

Conclusion: Our data revealed that valsartan as a type I angiotensin receptor antagonist could decrease oxidative stress and inflammation due to renal ischemia reperfusion injury. Hence, valsartan could propose as a therapeutic agent for kidney diseases such as renal ischemia-reperfusion injury regarded to these renoprotective effects.


Citation: Mohmoodnia L, Safari S, H, Koushki S, Farzan B, Papi S, Hadian B, et al. Antioxidative and anti-inflammatory of valsartan against renal ischemia-reperfusion injury; role of nitric oxide signaling pathway. Immunopathol Persa. 2019;5(2):e19. DOI:10.15171/ ipp.2019.19.
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