Fig. 7: Schematic diagram of the mechanisms by which BBR ameliorates the blockade of autophagic flux induced by cholesterol overloading.

BBR could (1) down-regulate SCP2 and inhibit cholesterol trafficking toward plasma membrane; (2) activate CYP7A1 expression and induce bile acid synthesis; and (3) mitigate COX2-mediated prostaglandin synthesis, which together led to the inhibition of AKT/mTOR phosphorylation and improved autophagic flux