| ORIGINAL ARTICLE |
|
| Year : 2020 | Volume
: 10
| Issue : 9 | Page : 397-402 |
|
|
Resveratrol downregulates TGF-β1 and Smad3 expression and attenuates oxidative stress in CCl4-induced kidney damage in rats
Saeed Mohammadi1, Jamshid Karimi2, Heidar Tavilani1, Iraj Khodadadi1, Roohollah Mohseni3, Mohammad Hashemnia4
1 Department of Clinical Biochemistry, Hamadan University of Medical Sciences, Hamadan, Iran
2 Department of Clinical Biochemistry; Nutrition Health Research Center, Hamadan University of Medical Sciences, Hamadan, Iran
3 Clinical Biochemistry Research center, Basic Health Sciences Institute, Shahrekord University of Medical Sciences, Shahrekord, Iran
4 Department of Pathobiology, Veterinary Medicine Faculty Razi University, Kermanshah, Iran
Correspondence Address:
Jamshid Karimi
Department of Clinical Biochemistry; Nutrition Health Research Center, Hamadan University of Medical Sciences, Hamadan
Iran
 Source of Support: This study was financially supported by the Hamadan University of
Medical Sciences (No: 9603302213), Conflict of Interest: None  | 16 |
DOI: 10.4103/2221-1691.290130
|
|
|
Objective: To evaluate the effect of resveratrol against CCl4- induced nephrotoxicity.
Methods: Forty-two male Wistar rats were divided into seven groups randomly. After six weeks, kidney weight, body weight, blood urea, serum creatinine, oxidative stress markers, and gene expression of renal transforming growth factor-beta1 (TGF-β1), TGF-β receptor type 1 (TGF-βR1) and Smad3 were determined. In addition, the protein level of TGF-β1 in the tissue lysate was measured.
Results: Resveratrol had a protective role in renal tissue by the improvement of antioxidant balance and reduction of renal parameters such as creatinine and urea (P<0.001). In addition, the renal mRNA level of TGF-β1, TGF-βRl, Smad3, as well as the protein level of TGF-β1 were decreased in rats treated with resveratrol (P<0.001), compared to the CCl4 group.
Conclusions: Overall, resveratrol shows a protective effect against nephrotoxicity in CCl4 treated rats by reducing oxidative stress status and modulating the TGF-β signaling. |
|
|
|
| [FULL TEXT] [PDF]* |
|
 |
|
