Alisol B 23-acetate is an agonist of farnesoid X receptor (FXR) [1].

FXR is a member of the nuclear receptor superfamily of ligand-activated transcription factors, playing a critical role in liver regeneration. Alisol B 23-acetate activates FXR-mediated regulation of genes involved in hepatocyte proliferation, potentially becoming a novel therapeutic option for facilitating efficient liver regeneration in patients subjected to liver resection [1].

In HepG2 cells transiently cotransfected with FXR expression plasmid, and FXR target gene,  bile salt export pump (BSEP) promoter reporter vector, Alisol B 23-acetate at doses of 0.1, 1 and 10 μM significantly increased luciferase activity. Additional increases were detected in cells treated with higher doses and reached a highest increase (4.3-fold) in cells treated with 10 μM of Alisol B 23-acetate [1].

In male C57BL6 mice received partial hepatectomy, Alisol B 23-acetate treatment (12.5, 25 or 50 mg/kg/d, p.o., for 7 days) significantly increased the ratio of liver regrowth, in a dose-dependent manner. In addition, significant increases in hepatocyte DNA synthesis and mitotic index could also be observed in Alisol B 23-acetate-treated mice, indicating that Alisol B 23-acetate promoted liver regeneration via enhancing hepatocyte proliferation [1].

Reference:

[1]. Meng Q, Chen X, Wang C, et al. Alisol B 23-acetate promotes liver regeneration in mice after partial hepatectomy via activating farnesoid X receptor. Biochemical Pharmacology, 2014, 92(2): 289-298.