Fig. 6

Schematic diagram illustrating the principal mechanism of EGCG and EC in the DNL pathway-mediated apoptosis in HepG2 cells. EGCG and EC decrease the expression of enzymes in DNL pathway including ACC and FASN, which is then results in reducing free fatty acid levels. The possible mechanisms of the anti-DNL pathway of EGCG and EC may be resulted from inhibition of EGCG on the tyrosine kinase receptor mediating PI3K/Akt/mTORC1/SREBP1 axis [28, 39, 42]. Subsequently, reduction of free fatty acid exhibits inhibition of mitochondrial CPT-1 activity, thereby contributing to disruption of lipid β-oxidation [18]. This inhibition results in promoting an increase of ceramide levels. As a result, ceramide can promote mitochondrial dependent apoptosis by activating the interaction of Bcl2 and BNIP3 [16, 54]. In addition, accumulation of ROS due to mitochondrial dysfunction and NADPH accumulation contributes to apoptosis in HepG2 [60]