Fig. 7

Model for the function of combined treatment of T0 and MGF in the AS related dyslipidemia targeting autophagy in cholesterol efflux from macrophage foam cells. On the one hand, T0 alone or T0 and MGF promote macrophage cholesterol efflux by activating LXRα to augment the expression of ABCA1 and ABCG1 and also enhance lipophagy in atherosclerotic lesion. Of note, in mammalian macrophage foam cells, lipid droplets are tagged for autophagic fusion, possibly beginning with mTOR-AMPK signaling to initiate lipid droplet degradation for further cholesterol depletion. On the other hand, T0-induced hepatic lipid abnormal accumulation is attenuated by MGF. In this scenario, MGF may activate AMPK signaling to suppress lipid synthesis and accelerate lipolysis for β-oxidation of free fatty acid. Alternatively, hepatic lipid droplets may be degraded through autophagy mechanism mediated by AMPK, and relative classical factors LC3, ATGs and p38 to facilitate hepatic lipophagy