Astragalus injection ameliorates cisplatin-induced nephrotoxicity in mice.
- Author:
Ling LIU
1
;
Juanjuan ZHANG
;
Ruiling HE
;
Liming ZHOU
;
Jie ZHANG
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Antineoplastic Agents; toxicity; Astragalus Plant; Cisplatin; toxicity; Injections; Kidney; drug effects; pathology; Male; Mice; Neoplasms, Experimental; drug therapy; Phytotherapy; Proto-Oncogene Proteins c-bcl-2; analysis; bcl-2-Associated X Protein; analysis
- From: China Journal of Chinese Materia Medica 2010;35(20):2736-2740
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo examine the protective effects of Astragalus injection (AI) on cisplatin (DDP)-induced nephrotoxicity and to explore the mechanism of its nephroprotection.
METHODThe S180-bearing model was established, and fifty mice were randomly divided into five groups: control mice, DDP-injected mice (3.5 mg x kg(-1)) and AI-pretreated mice (12, 8, 4 g x kg(-1)). Tumor inhibition rate, renal functions, histological findings were investigated. The apoptotic cells were counted by TUNEL and the presence of Bax, Bcl-2 in renal tissues was determined by immunohistochemistry.
RESULTSAdministration of DDP or DDP plus AI showed promising anti-tumor activities as compared with control group. Interestingly, a combination of DDP and AI (12, 8 g x kg(-1)) led to enhanced tumor growth inhibition as compared with DDP alone (all P < 0.05). Compared with that from control, the number of TUNEL-positive cells and the Bax/Bcl-2 ratio was increased significantly in the kidneys of DDP treated mice (P < 0.05). High-dose AI pretreatment significantly reduced the elevated number of TUNEL-positive cells and the Bax/Bcl-2 ratio (P < 0.05), and it showed a superior nephroprotective effect than any other dose. AI significantly also decreased both the damage to renal function and histological pathology.
CONCLUSIONPre-treatment with AI attenuates cisplatin-induced nephrotoxicity without compromising the anti-tumor efficacy of DDP, which might be involved in regulating the Bax and Bcl-2 expression.