Asperuloside Inhibits Cell Viability and Induce Apoptosis in Liver Cancer HepG2 Cells via Inhibiting PI3K/AKT/mTOR Pathway

Abstract

Liver cancer, a formidable global health issue, is characterized by its high mortality rates, making it the third major cause of cancer-associated deaths worldwide. The 5-year survival rate for liver cancer remains dismally low, particularly in advanced stages, emphasizing an urgent need for more effective therapeutic methods. The present study evaluated how asperuloside eliminates liver cancer cells by inhibiting viability and enhancing apoptosis in HepG2 cells. An MTT assay was employed to evaluate the effect of asperuloside on the proliferation of liver cancer HepG2 cells. The asperuloside-induced cell damage in the HepG2 cells was evaluated by the lactate dehydrogenase (LDH) release assay utilizing kits. The apoptotic levels in the HepG2 cells were examined using a dual staining technique. The levels of phosphatidylinositol 3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/AKT/mTOR) pathway proteins in the untreated and asperuloside-treated HepG2 cells were assessed using kits. The MTT assay results indicated a notable decrease in HepG2 cell growth after treatment with diverse concentrations of asperuloside. Asperuloside treatment induced cell damage in the HepG2 cells, as evidenced by increased LDH activity. The findings of the dual staining assay confirmed the initiation of apoptosis in the asperuloside-exposed HepG2 cells. Moreover, the asperuloside treatment markedly decreased the PI3K, AKT, and mTOR levels in the HepG2 cells. The present findings indicate that asperuloside significantly inhibits viability and promotes apoptosis in liver cancer HepG2 cells via downregulating the PI3K/AKT/mTOR pathway. Consequently, it possesses the capacity to serve as an effective anti-cancer agent to treat liver cancer.