Supplementation of BC2000 and Ellagic Acid Inhibits High-Fat-Induced Hypercholesterolemia by Promoting Liver Primary Bile Acid Biosynthesis and Intestinal Cholesterol Excretion in Mice.

The probiotic () BC2000 can increase the abundance of intestinal transforming ellagic acid (EA) bacteria and inhibit metabolic disorders caused by hyperlipidemia by activating liver autophagy. This study aimed to investigate the inhibitory effects of BC2000 and EA on hyperlipidemia-induced cholesterol metabolism disorders. C57BL/6J mice ( = 10 in each group) were fed a low-fat diet, high-fat diet (HFD), HFD supplemented with EA, HFD supplemented with EA and BC77, HFD supplemented with EA, and BC2000. EA and BC2000 supplementation prevented HFD-induced hypercholesterolemia and promoted fecal cholesterol excretion. Transcriptome analysis showed that primary bile acid biosynthesis in the liver was significantly activated by EA and BC2000 treatments. EA and BC2000 treatment also significantly increased the intestinal abundance and the liver EA metabolites, iso-urolithin A, Urolithin A, and Urolithin B. Therefore, BC2000 supplementation promoted the intestinal transformation of EA, which led to the upregulation of liver bile synthesis, thus preventing hypercholesterolemia.