Chenodeoxycholic Acid-mediated Activation of the Farnesoid X Receptor Negatively Regulates Hydroxysteroid Sulfotransferase
作者： Masaaki Miyata , Yoshiki Matsuda , Hiroyuki Tsuchiya , Hirotaka Kitada , Takanori Akase
DOI: 10.2133/DMPK.21.315
关键词:
摘要: Summary: Hydroxysteroid sulfotransferase catalyzing bile acid sulfation plays an essential role in protection against lithocholic (LCA)-induced liver toxicity. Hepatic levels of Sult2a is up to 8-fold higher farnesoid X receptor-null mice than the wild-type mice. Thus, influence FXR ligand (chenodeoxycholic (CDCA) and LCA) feeding on hepatic expression was examined FXR-null protein content elevated fed a LCA (1% 0.5%) diet. Treatment with 0.5% CDCA diet decreased 20% control mice, but increased Liver Sult2a1 (St2a4) mRNA were reduced 26% after diet, while no decrease observed feeding. A significant inverse relationship (r 2 = 0.523) found between small heterodimer partner (SHP) level. PCN-mediated increase attenuated by not Human SULT2A1 HepG2 cells treated agonists, or GW4064 dose-dependent manners, although SHP increased. These results suggest that SULT2A negatively regulated through CDCA-mediated activation humans.
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