Lappaconitine Hydrochloride Induces Apoptosis and S Phase Cell Cycle Arrest through MAPK Signaling Pathway in Human Liver Cancer HepG2 Cells

Objectives: The objective of this study was to examine the antitumor effect and primary mechanisms of LH on cell proliferation, cell cycle, and apoptosis in HepG2 cells. Materials and Methods: The cell viability and proliferation were assessed using Cell Counting Kit‑8 and 5’‑ethynyl‑2’‑deoxyuridine assay. The apoptosis morphological feature of cell was detected with the 4’,6-diamidino-2- phenylindole (DAPI) staining method. The effect of protein expression levels was recognized by Western blot assay. Cell cycle and apoptosis were estimated using flow cytometer. Results: LH repressed cell viability and proliferation of HepG2 cells and persuaded apoptosis in a dose‑dependent way. Flow cytometry analysis results display that LH could arrest cell cycle of HepG2 cells in S phase, thereby preventing cells entering G2/M phase. LH upregulated the expression of cytochrome C, Bax, P53, cleaved caspase‑3, cleaved caspase‑9, and cleaved poly ADP-ribose polymerase (PARP) and suppressed the expression of Bcl‑2. Furthermore, caspase inhibitor z‑VAD‑fmk inhibited the activation of cleaved caspase‑3 and cleaved caspase‑9. Moreover, LH abridged the phosphorylation levels of extracellular signal‑regulated kinase and augmented the phosphorylation levels of c‑Jun N‑terminal kinase and P38. Conclusion: LH designated antitumor effect against HepG2 cells through suppressing cell proliferation, inducing apoptosis and cell cycle arrest by aiming mitogen‑activated protein kinase signaling pathway.