Diallyl trisulfide induces pro-apoptotic autophagy via the AMPK/SIRT1 signalling pathway in human hepatocellular carcinoma HepG2 cell line

Background: Liver cancer is associated with a high mortality rate worldwide. Hepatocellular carcinoma (HCC) constitutes large proportion of primary liver cancers, and most its alterations currently remain untreatable. Diallyl trisulfide (DATS), the main chemical constituent allicin, affects tumour development by regulating cell apoptosis. Allicin-induced autophagy could contribute to apoptosis in HepG2 cells. We rigorously examined autophagy-related mechanism allicin-induced treated cells DATS explore effect on pro-apoptotic lines examine specific molecular mechanism.
 Methods: were various concentrations for 24 48 h. Subsequently, viability was measured using counting kit-8 (CCK-8) assay clone formation assay. The Hoechst 33258 staining western blotting. Autophagy AMP-activated protein kinase (AMPK)/NAD-dependent deacetylase sirtuin-1 (SIRT1) signalling pathway detected blotting.
 Results: Our results indicated that inhibited growth. Moreover, ability promote increased increasing concentration. verified phenomenon DATS-induced demonstrated treatment upregulated expression LC3-II/I. By measuring potential stimulators, we documented induce activating AMPK/SIRT1 pathway.
 Conclusion: induced via human HCC line. findings further implicate allicin as therapeutic agent against tumours clinical settings, providing basis combining an agonist treating cancer.