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Articles in PresS, published online ahead of print March 28, 2002
Am J Physiol Gastrointest Liver Physiol, 10.1152/ajpgi.00536.2001
Submitted on December 21, 2001
Accepted on March 23, 2002
1 Department of Medicine, Rhode Island Hospital and Brown University School of Medicine, Providence, RI, USA
* To whom correspondence should be addressed. E-mail: Zuo-Liang_Xiao_MD{at}brown.edu.
Hydrophobic bile acids impair gallbladder emptying in vivo and inhibit gallbladder muscle contraction in response to CCK-8 in vitro. This study was aimed at determining the mechanisms of muscle cell dysfunction caused by bile acids in guinea pig gallbladders. Muscle cells were obtained by enzymatic digestion. TCDC, a hydrophobic bile acid, caused a contraction of up to 15% and blocked CCK induced contraction. Indomethacin abolished the TCDC induced contraction. Hydrophilic bile acid TUDC had no effect on muscle contraction but prevented the TCDC induced contraction and its inhibition on CCK induced contraction. Pretreatment with NADPH oxidase inhibitor PH2I, xanthine oxidase inhibitor allopurinol and free radical scavenger catalase also prevented TCDC induced contraction and its inhibition of the CCK induced contraction. TCDC caused H2O2 production, lipid peroxidation and increased PGE2 synthesis and activities of catalase and SOD. These changes were significantly inhibited by pretreatment of Ph2I or allopurinol. Inhibitors of cPLA2, PKC and MAPK also blocked the TCDC induced contraction. It is concluded that hydrophobic bile acids cause muscle cell dysfunction by stimulating the formation of H2O2 via activation of NADPH and xanthine oxidase. H2O2 causes lipid peroxidation and activates cPLA2 to increase PGE2 production that in turn stimulates the synthesis of free radical scavengers through PKC-MAPK pathway.
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