Silibinin alleviates N-nitrosodimethylamine-induced glutathione dysregulation and hepatotoxicity in rats.
10.3724/SP.J.1009.2016.00040
- Author:
Devaraj EZHILARASAN
1
;
Sivanesan KARTHIKEYAN
2
Author Information
1. Food and Hepatotoxicology Laboratory, Department of Pharmacology and Environmental Toxicology, University of Madras, Taramani, Chennai 600113, India.
2. Food and Hepatotoxicology Laboratory, Department of Pharmacology and Environmental Toxicology, University of Madras, Taramani, Chennai 600113, India. Electronic address: hepatotoxicology.lab@gmail.com.
- Publication Type:Journal Article
- Keywords:
Dimethylnitrosamine;
Glutathione dysregulation;
Hepatotoxicity;
Oxidative stress;
Silibinin
- MeSH:
Animals;
Antioxidants;
pharmacology;
Chemical and Drug Induced Liver Injury;
drug therapy;
Dimethylnitrosamine;
toxicity;
Female;
Glutathione;
metabolism;
Male;
Protective Agents;
pharmacology;
Rats;
Rats, Wistar;
Silybin;
Silymarin;
pharmacology
- From:
Chinese Journal of Natural Medicines (English Ed.)
2016;14(1):40-47
- CountryChina
- Language:English
-
Abstract:
The present study was designed to evaluate the hepatoprotective and antioxidant potentials of silibinin (SBN) against N-nitrosodimethylamine (DMN)-induced toxic insults in the rat liver. The liver damage was induced in Wistar albino rats by repeated administration of DMN (10 mg·kg(-1) b.w., i.p.) on 3 consecutive days per week for 3 weeks. SBN (100 mg·kg(-1) b.w., p.o.) was given daily to the DMN treated rats for two weeks. The marker enzymes of liver toxicity and second-line enzymic and non-enzymic antioxidants were evaluated in serum and liver tissues before and after SBN treatment. Histopathology of the liver was evaluated by H & E staining. The DMN treatment produced a progressive increase in all the serum marker enzymes (AST, ALT, ALP, LDH, and γ-GT), peaking on Day 21. This treatment produced highly significant decreases in all the second-line antioxidant parameters (GSH, GST, GR, GPx, and vitamins C and E). The SBN treatment significantly reversed the DMN-induced damages, towards normalcy. Histopathological studies confirmed the development of liver toxicity in DMN-treated rats, which was reversed by SBN treatment in corroboration with the aforementioned biochemical results, indicating the hepatoprotective and antioxidant properties of SBN. In conclusion, the DMN-induced degenerative changes in the liver were alleviated by SBN treatment and this protective ability may be attributed to its antioxidant, free radical scavenging, and membrane stabilizing properties.
