Accordingly, for the atherosclerosis apoE−/− mice model, CGE decreased their lipid levels and improved liver lipid deposition, liver lesions, and aortic plaques, suggesting that CGE can regulate lipid metabolism and cholesterol synthesis, as well as lipid transportation by upregulating the PPAR-γ-LXR-α-ABCA1 signaling pathways associated with reverse cholesterol transport. This evidence concerns the gene PPARG and atherosclerosis.