EVALUATION OF LIPID PROFILE NATURE OF SOLANUM XANTHOCARPUM LEAVES IN DIETHYLNITROSAMINE INDUCED HEPATOCELLULAR CARCINOGENESIS ON WISTAR RATS

Periyannan Velu; Perumal Iyappan

Volume : V, Issue : III, March - 2015

EVALUATION OF LIPID PROFILE NATURE OF SOLANUM XANTHOCARPUM LEAVES IN DIETHYLNITROSAMINE INDUCED HEPATOCELLULAR CARCINOGENESIS ON WISTAR RATS

Periyannan Velu, Perumal Iyappan

Abstract :

Antioxidants are one of the key role players in carcinogenesis, several natural antioxidants were shown to have anticancer effects. In the present investigation the efficacy of Solanum xanthocarpum(SXC) Schrad&Wendl on the antioxidant status of Diethylnitrosamine (DEN) induced liver carcinogenesis in male Wistar albino rats were assessed. The rats were divided into six groups. The rats in the group 1 and 2 were normal control and SXC aqueous leaves extract control respectively. Groups 3, 4, 5 and 6 were administered with DEN (0.01%) in drinking water for 16 weeks to induce hepatocellular carcinoma (HCC). Starting one week prior to DEN administration group 4, 5 and 6 rats were treated with SXC aqueous leaves extract (75, 150 and 300mg/kg bw) day in diet for 16 weeks. After the experimental period of serum glutamic oxaloacetic acid–transaminase (SGOT) and serum glutamic phosphoacetic acid–transaminase (SGPT), alkaline phosphatase (ALP), albumin, bilirubin, total protein, triglycerides (TG), cholesterol (CL) and high density lipoprotein (HDL). In contrast, SXC aqueous leaves extract with DEN treated group 4, 5 and 6 animals showed a significant decrease in the number of nodules with concomitant decrease in the biochemical status. The activities of biochemical analysis liver were improved when compared with hepatocellular carcinoma (HCC) induced group 3 rats. In the present study biochemical analysis were also carried out which supports the chemopreventive action of the SXC aqueous leaves extract against DEN administration during liver cancer progression. These findings suggest that SXC aqueous leaves extract suppresses DEN induced hepatocarcinogenesis by modulating the antioxidant defence status of the rats.