Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

Polydatin ameliorates renal fibrosis in a streptozotocinâ€“induced rat model of diabetic nephropathy by inhibiting TLR4/NF-κB signaling

Huimin Niu¹ , Gang Li², Yanhong Qiao¹, Feng Wang¹

¹Department of Nephrology, Heping Hospital affiliated to Changzhi Medical College.Changzhi, Shanxi 046000, China; ²Department of Urology, Heji Hospital affiliated to Changzhi Medical College, Changzhi, Shanxi 046011, China.

For correspondence:- Huimin Niu Email: NiuhuiminatHJH@163.com Tel:+863553128406

Accepted: 17 October 2019 Published: 30 November 2019

Citation: Niu H, Li G, Qiao Y, Wang F. Polydatin ameliorates renal fibrosis in a streptozotocinâ€“induced rat model of diabetic nephropathy by inhibiting TLR4/NF-κB signaling. Trop J Pharm Res 2019; 18(11):2263-2269 doi: 10.4314/tjpr.v18i11.5

© 2019 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..

Abstract

Purpose: To determine the effects of polydatin (PD) on a streptozotocin (STZ)-induced rat model of diabetic nephropathy (DN) and NRK-52E cells treated with high glucose (HG).

Methods: Sprague Dawley rats received 65 mM STZ to model DN in vivo. NRK-52E cells were treated with HG, to model DN in vitro. Both models were treated with PD. Fasting blood glucose, kidney/body weight, urinary protein, serum creatinine, and blood urea nitrogen levels, interstitial injury score, as well as protein expression levels of connective tissue growth factor (CTGF), fibronectin, and collagen I were determined in DN rats after PD treatment. Enzyme-linked immunosorbent assay was used to measure inflammatory factors. Protein expression was determined by Western blot analysis while apoptosis was assessed by flow cytometry.

Results: STZ successfully induced DN in rats. PD treatment significantly reduced kidney/body weight; decreased fasting blood glucose, urinary protein, serum creatinine, and blood urea nitrogen levels; lowered interstitial injury scores; and downregulated protein expression levels of CTGF, fibronectin, and collagen I. It also inhibited inflammatory reaction and suppressed Toll-like receptor (TLR4)/nuclear factor (NF)-κB signaling. Furthermore, PD suppressed apoptosis, reduced inflammatory factor levels, and suppressed TLR4/NF-κB signaling induced by HG in NRK-52E cells.

Conclusion: PD exerts a protective role in DN by decreasing interstitial injury, reducing renal fibrosis, inhibiting inflammatory responses, and suppressing cell apoptosis, at least, partly via inactivation of TLR4/ NF-κB pathway.

Keywords: Polydatin, Diabetic nephropathy, Streptozotocin, NRK-52E, TLR4/NF-κB pathway