Studies of some Egyptian medicinal plants as natural wealth in regression of hepatocellular carcinoma [HCC]

The present investigation was designed to valuate the antiangiogenic efficacy of some local medicinal plants against liver cancer induced by diethylnitrosamine [DEN] methanolic extracts of cupressus sempervirens, chelidonium majus and tropaeolum majus were used in this study. Vascular endothelial growth factor [VEGF], alpha-Feto-protein [AFP], ferritin, alanine transaminase [ALT], aspartate transaminase [AST], Alkaline phosphatase [ALP], superoxide dismutase [SOD] and Glutathione peroxidase [GPx] were determined in blood while Nitric oxide [NO] was determined in liver tissue homogenate. Furthermore histopathological investigations ere done. The results showed that the treatment with methanolic extracts of all selected plants led to a significant reduction in the level of all the desired biochemical parameters, while the administration of cupressus sempervirens only improved the histopathological pictures of liver architecture. These results suggest a beneficial effect of these plant extracts against experimentally-induced hepatocellular carcinoma and the possible mechanism of the protective effects may be partly due to the antioxidant activity of these plants

Evaluation of protective potentials of a potentized homeopathic drug, Chelidonium majus, during azo dye induced hepatocarcinogenesis in mice.

Several cytogenetical and enzymatic protocols were used to test if two microdoses of Chelidonium majus, namely Chelidonium-30 (Ch-30) and Chelidonium-200 (Ch-200), used as homeopathic drugs, showed anti-tumor activity and also favorably modulated genotoxic damages produced by an azo dye in mice at several intervals of fixation. Different sets of healthy mice were fed: (i) hepatocarcinogen, p-dimethylaminoazobenzene (p-DAB, initiator) + phenobarbital (PB, promoter), (ii) only p-DAB, (iii) only PB, and (iv) neither p-DAB nor PB (normal control). Mice fed with p-DAB + PB were divided into different sets that were also fed either Ch-30 (v) or Ch-200 (vi) or diluted alcohol (vii), the "vehicle" of the microdoses of Chelidonium. All mice of group (i), a few of group (ii) and group (vii) and none of groups (iii) and (iv) developed tumors in liver at the longer intervals of fixation. The frequencies of chromosome aberrations (CA), micronucleated erythrocytes (MN), mitotic index (MI) and sperm head abnormality (SHA) were much higher in groups (i) and (vii) mice than in groups (ii), (iii) and (iv) mice at all fixation intervals. However, in mice of both groups (v) and (vi), the frequencies of CA, MN, SHA were strikingly less than those of groups (i) and (vii), and moderately less than those of groups (ii) and (iii). Both Ch-30 and Ch-200 also modulated favourably some toxicity marker enzymes like acid and alkaline phosphatases, peroxidases, glutamate oxaloacetate and glutamate pyruvate transaminases in liver, kidney and spleen tissues of the carcinogen fed mice. The microdoses of Chelidonium having no visible ill effects of their own, may be strong candidates for use in delaying/protecting liver cancer.