Biliary cholesterol may contribute to the formation of cholesterol gallstones, regulation of these levels could be a useful therapeutic strategy for gallstones disease. Piperine （PA） is a potential cholesterol lower...Biliary cholesterol may contribute to the formation of cholesterol gallstones, regulation of these levels could be a useful therapeutic strategy for gallstones disease. Piperine （PA） is a potential cholesterol lowering a- gent. In this study, we assessed the effect and mechanism of PA in preventing cholesterol gallstones formation in- duced by feeding lithogenic diet containing high cholesterol levels to mice. C57BL/6 inbred mice were fed lithogen- ic or chow diets for 10 weeks, with or without PA （ 15, 30 and 60 mg ~ kg-1 ） or ursodeoxycholic acid （ UDCA, 60 mg ~ kg-1） administration. Cholesterol, phospholipids and crystals in bile, the lipid in serum, pathological chan- ges and proteins expression in liver were analyzed. The results showed that PA could decrease the cholesterol poten- cy and crystals in bile, reduce total cholesterol （TC）, triglycerides （TG） and increase high-density lipoprotein / low-density lipoprotein （HDL/LDL） levels in serum. Furthermore, PA treatment reduced liver lipid peroxidation and protected hepatobiliary cells from liver injury by decreasing malondialdehyde （MDA） and increasing superoxide dismutase （SOD）. In addition, PA inhibited the expression of ATP-binding cassette transporters G5/8 （ABCG5/ 8 ） and liver X receptor （LXR） in liver, and reduced cholesterol transport from the hepatocytes to the gallbladder. It may be the mechanism of PA in preventing cholesterol gallstones formation. PA as a potential drug for prevention cholesterol gallstones merits further investigation.展开更多
文摘Biliary cholesterol may contribute to the formation of cholesterol gallstones, regulation of these levels could be a useful therapeutic strategy for gallstones disease. Piperine （PA） is a potential cholesterol lowering a- gent. In this study, we assessed the effect and mechanism of PA in preventing cholesterol gallstones formation in- duced by feeding lithogenic diet containing high cholesterol levels to mice. C57BL/6 inbred mice were fed lithogen- ic or chow diets for 10 weeks, with or without PA （ 15, 30 and 60 mg ~ kg-1 ） or ursodeoxycholic acid （ UDCA, 60 mg ~ kg-1） administration. Cholesterol, phospholipids and crystals in bile, the lipid in serum, pathological chan- ges and proteins expression in liver were analyzed. The results showed that PA could decrease the cholesterol poten- cy and crystals in bile, reduce total cholesterol （TC）, triglycerides （TG） and increase high-density lipoprotein / low-density lipoprotein （HDL/LDL） levels in serum. Furthermore, PA treatment reduced liver lipid peroxidation and protected hepatobiliary cells from liver injury by decreasing malondialdehyde （MDA） and increasing superoxide dismutase （SOD）. In addition, PA inhibited the expression of ATP-binding cassette transporters G5/8 （ABCG5/ 8 ） and liver X receptor （LXR） in liver, and reduced cholesterol transport from the hepatocytes to the gallbladder. It may be the mechanism of PA in preventing cholesterol gallstones formation. PA as a potential drug for prevention cholesterol gallstones merits further investigation.
