摘要
Background: Polysaccharides extracted from the medicinal herbs are known to possess antitumor effects. Although there is a significant number of evidences implicated on the beneficial effects of the ginseng leaves ginsenoside with diverse associated mechanisms, reports on the anticancer by the ginseng leaves crude polysaccharides (GLCP) are not sufficient. Experiments were carried out to unravel the anticancer effects of GLCP. Methods: Cells were treated with GLCP (0.5 - 2 mg/ml) for 48h. MTT method was used to detect the cell viability. Western blot and flow cytometry were used to detect apoptotic rate. Western blot and acridine orange staining were used to detect the cell autophagy. Results: Compared with the normal human liver cell (Chang liver), GLCP (1.5 - 2 mg/ml) significantly reduction cell viability, promote apoptosis-related proteins expression, promote cell apoptosis and autophagy in SMMC-7721 cells. But caveolin-1 gene silencing could inhibit the anticancer effect of GLCP. Conclusions: These data suggest that GLCP promote autophagy and apoptosis in human hepatoma cell SMMC-7721. We speculate that its mechanism may be associated with the caveolin-1 which is an essential structural molecule of caveolae. Although the effect of GLCP inhibited of liver cancer is not very strong, we are more interested in the GLCP which plays a tumor suppressor role in health care.
Background: Polysaccharides extracted from the medicinal herbs are known to possess antitumor effects. Although there is a significant number of evidences implicated on the beneficial effects of the ginseng leaves ginsenoside with diverse associated mechanisms, reports on the anticancer by the ginseng leaves crude polysaccharides (GLCP) are not sufficient. Experiments were carried out to unravel the anticancer effects of GLCP. Methods: Cells were treated with GLCP (0.5 - 2 mg/ml) for 48h. MTT method was used to detect the cell viability. Western blot and flow cytometry were used to detect apoptotic rate. Western blot and acridine orange staining were used to detect the cell autophagy. Results: Compared with the normal human liver cell (Chang liver), GLCP (1.5 - 2 mg/ml) significantly reduction cell viability, promote apoptosis-related proteins expression, promote cell apoptosis and autophagy in SMMC-7721 cells. But caveolin-1 gene silencing could inhibit the anticancer effect of GLCP. Conclusions: These data suggest that GLCP promote autophagy and apoptosis in human hepatoma cell SMMC-7721. We speculate that its mechanism may be associated with the caveolin-1 which is an essential structural molecule of caveolae. Although the effect of GLCP inhibited of liver cancer is not very strong, we are more interested in the GLCP which plays a tumor suppressor role in health care.
