Abstract
An effectual remedy for hepatocellular carcinoma (HCC) and knowledge of the mechanism are urgently needed. Researchers have found that CPhGs, an extract from Cistanche tubulosa (Schenk) Wight, had better antitumor effects, but its mechanism is still unknown. In the present study, using an H22 tumor-bearing mouse as a model, we investigated the antitumor effects of CPhGs and the effect of CPhGs on autophagy and apoptosis. Besides, we also discussed the role of autophagy with the help of HCQ and rapamycin. Our results show that CPhGs inhibit tumor growth and induce apoptosis and autophagy of tumor tissue. TUNEL staining displayed that tumor apoptosis rate increased after the intervention of CPhGs, and immunohistochemistry and western blot showed that cleaved-PARP and cleaved-caspase 3 were upregulated after the intervention of CPhGs, and these results were most pronounced in the high-dose group. Autophagy results revealed that CPhGs increased the number of autophagosomes, increased the level of LC3B-II, and decreased the level of p62. Finally, our results showed that excessive autophagy suppresses tumor growth, whereas inhibition of autophagy does the opposite, which indicated that CPhGs induced autophagic death in H22 hepatoma-bearing mice. These data altogether confirmed the involvement of apoptosis and autophagy in CPhGs treatment for HCC.