Effects of ginsenoside Rg1 on streptozocin-induced diabetic nephropathy in rats.
- Author:
Xiaofen MA
1
;
Xisheng XIE
;
Chuan ZUO
;
Junming FAN
Author Information
1. Department of Nephrology, West China Hospital of Sichuan University, Chengdu 610041, China.
- Publication Type:Journal Article
- MeSH:
Animals;
Diabetes Mellitus, Experimental;
complications;
Diabetic Nephropathies;
drug therapy;
Drugs, Chinese Herbal;
therapeutic use;
Ginsenosides;
therapeutic use;
Male;
Phytotherapy;
RNA, Messenger;
genetics;
metabolism;
Random Allocation;
Rats;
Rats, Sprague-Dawley;
Transforming Growth Factor beta1;
genetics;
metabolism
- From:
Journal of Biomedical Engineering
2010;27(2):342-347
- CountryChina
- Language:Chinese
-
Abstract:
This study sought to assess the effect of Ginsenoside Rg1 on streptozocin-induced diabetic nephropathy in rats and to unveil the underlying mechanism. Diabetic nephropathy (DN) was induced by intraperitoneal injection of streptozocin (STZ). Eight weeks after drug administration, the rats from each group were sacrificed. Serum creatine (Scr) and 24 hours urine protein, cross reaction protein (CRP) and tumor necrosis factor-alpha (TNF-alpha) were measured at the end of the study. The histological changes of renal interstitial tissues were observed by periodic acid-Schiff staining (PAS). Immunohistochemical method was used to examine the expression levels of ectodermal dysplasia (ED-1). The mRNA of transforming growth factor-beta1 (TGF-beta1) was measured by real-time PCR (RT-PCR), and the protein expression of TGF-beta1 was surveyed by Enzyme-Linked Immunosorbent Assay (ELISA). The renal pathological changes in DN rats given ginsenoside Rg1 treatment were ameliorated, and the expression levels of 24 h urine protein, serum creatinine, CRP, TNF-alpha, ED-1 and TGF-beta1 were significantly lower than those in the diabetic nephropathy group (P < 0.05). So, we reach a conclusion that, in the experiment, Ginsenoside Rg1 obviously reduced TGF-beta1 expression and the already-mentioned inflammatory reaction factors in the renal tissues and improved the renal pathological changes in DN rats.
