Basic & Clinical Medicine ›› 2014, Vol. 34 ›› Issue (7): 984-989.

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Increased bile cholesterol content inhibits the gallbladder contraction by affecting the re-distribution of CCK-1R

  

  • Received:2014-04-18 Revised:2014-05-16 Online:2014-07-05 Published:2014-06-24

Abstract: Objective To analyze the relationship between bile total cholesterol (TC) content and the contraction of the gallbladder, and to explore its possible mechanism. Methods A total of 73 patients with or without gallstones, who underwent biliary surgery in the Department of General Surgery in PUMCH from March 2013 to January 2014, were selected and divided into gallstone group and non-gallstone group. The bile of all these patients was collected during the operation, and the content of the bile TC and total bile acid (TBA) was detected. The gallbladder contraction test in patients with gallstones was performed before the surgery. The expression of cholecystokinin-1 receptor (CCK-1R) and caveolin-3 (Cav-3) in gallbladder mucosa and the smooth muscle in two groups was detected using immunohistochemistry staining method. The co-localization of CCK-1R and Cav-3 in gallbladder mucosa and the smooth muscle in two groups was also observed using immunofluorescence method. Results The content of bile TC and TBA in patients with gallstones was significantly higher than that in patients without gallstones (P<0.05). And the bile TC content in patients with a worse contraction of the gallbladder was significantly higher than that in patients with a better contraction of the gallbladder (P<0.05). The immunohistochemistry staining revealed that the expression of Cav-3 in the gallbladder mucosa in gallstone group was significantly higher than that in non-gallstone group (P<0.05). The co-localization of CCK-1R and Cav-3 in gallstone groups was obvious in both gallbladder mucosa and the smooth muscle, while no obvious co-localization was observed in non-gallstone group. Conclusion The increased bile TC content can inhibit the contraction of the gallbladder, and the mechanism may relate to excess Cav-3 binding with CCK-1R, thus affecting the function of CCK.

Key words: Gallbladder, Cholesterol, Cholecystokinin receptor, Caveolin-3, Bile

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