Lesion scoring and P450 Isoenzyme activity in liver of hepatocarcinogenesis rats treated with Strobilanthes crispus

In this study, we have undertaken efforts to ascertain the anticancer potency of S.crispus (SC) extract on diethylnitrosamine (DEN) and acetylaminofluorene (AAF) induced HCC with special attention to hepatic drug metabolism and to investigate the effect of SC on preneoplastic marker enzyme activity specifically of microsomal aniline hydroxylase (AH) activity and lesion scoring in rats treated with DEN and AAF and controls. Thirty male Sprague Dawley rats were divided to six equal number groups. In the first three groups, hepatocellular carcinoma was induced with diethylnitrosamine and acetylaminofluorene. Three groups in each branch were randomly assigned to receive 5% w/v of SC extract, glycyrrhizin or no treatment. After 12 weeks of treatment, the rats were sacrificed. Lesion scoring analysis and Aniline hydroxylase assays were performed as outcome measures. The obtained results have shown a significant, increase (p<0.05) of liver microsome AH in cancer group rats after 12 weeks. Treatment with glycyrrhizin caused decrease in liver AH activity compared to control group. Meanwhile, treatment with SC caused overall decrease in liver AH activity almost near to control group. Meanwhile, microscopic observation of the lesion score during hepatocarcinogenesis revealed that cells of cancer group without treatment were severely necrotic at week 12. S. crispus treatment reduced the severity in cancer group rats at week 12. S. crispus only ameliorated the cancer incidence in the liver, however did not fully recover the liver tumor similar to the normal cells. This might be due to short experimental duration. The chemopreventive action may be due to the scavenging of the reactive oxygen radicals from the system, as well as inhibition of the enzymes responsible for the activation of DEN. In this study, SC extract may act as a chemopreventive agent which exerts its protective effects by inhibition of enzymes involved in metabolic activation of carcinogen (phase I enzyme i.e ANH)