EFFECTS OF THIOCIN ON 7Α-HYDROXYLASE ACTIVITY IN THE COURSE OF EXPERIMENTAL ATHEROSCLEROSIS DEVELOPMENT

Abstract

In the liver, cholesterol is converted into bile acids through the catalytic activity of cholesterol 7α-hydroxylase (CYP7A1), the rate-limiting enzyme in the classical bile acid synthesis pathway. The resulting bile acids are secreted into the biliary system and released into the gastrointestinal tract as components of bile, where they play an essential role in the emulsification and intestinal absorption of dietary lipids [4,2]. Cholesterol 7α-hydroxylase regulates the formation of 7α-hydroxycholesterol, the primary precursor of bile acids, thereby maintaining cholesterol homeostasis [5]. Consequently, CYP7A1 is considered one of the key enzymes controlling cholesterol catabolism and elimination from the body. Alterations in its activity may impair bile acid synthesis, promote cholesterol accumulation, and contribute to the development of dyslipidemia and atherosclerosis. Therefore, understanding the regulation of CYP7A1 is of considerable importance for elucidating the mechanisms underlying cholesterol metabolism and for developing novel therapeutic approaches to hypercholesterolemia, atherosclerosis, and other cardiovascular diseases [3].