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NEUROREGULATION AND MOTILITY

Role of PGE₂ on gallbladder muscle cytoprotection of guinea pigs

Department of Medicine, Rhode Island Hospital and Brown University School of Medicine, Providence, Rhode Island 02903

Submitted 30 May 2003 ; accepted in final form 19 August 2003

H₂O₂ and taurochenodeoxycholic acid (TCDC) impair the contraction induced by CCK-8, ACh, and KCl without affecting the actions of PGE₂ and damage functions of membrane proteins except for PGE₂ receptors. The aim of this study was to examine whether the preserved PGE₂ actions contribute to cytoprotective mechanisms against reactive oxygen species. Muscle cells from guinea pig gallbladder were obtained by enzymatic digestion. Levels of lipid peroxidation and activities of SOD and catalase were determined by spectrophotometry. Pretreatment with PGE₂ prevented the inhibition of H₂O₂ or TCDC on agonist (CCK-8, ACh, and KCl)-induced contraction and reduced the expected increase in lipid peroxidation and activities of catalase and SOD caused by H₂O₂ and TCDC. Incubation with CCK-8 for 60 min desensitized CCK-1 receptors up to 30 min, whereas no receptor desensitization was observed after PGE₂ pretreatment. Cholesterol-rich liposome treatment enhanced the inhibition of H₂O₂ and TCDC on agonists-induced contraction, including that of PGE₂. Pretreatment with PGE₂ before H₂O₂ and TCDC did not completely block their inhibition on agonist-induced contraction. Cholesterol-rich liposome treatment impaired the expected increase in catalase activities in response to PGE₂. We conclude that pretreatment with PGE₂ prevents the muscle cell damage caused by H₂O₂ and TCDC due to the resistance of PGE₂ receptors to agonist-induced desensitization. The preservation of PGE₂ receptors may be designed to conserve these cytoprotective functions that are, however, impaired by the presence of excess cholesterol in the plasma membrane.

reactive oxygen species; free radical scavengers; bile acids; receptor desensitization

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