EFFECT OF PREINDUCTION OF HEAT-SHOCK PROTEINS ON ACETIC ACID-INDUCED SMALL-INTESTINAL LESIONS IN RATS

Bowel dysfunction such as irritable bowel syndrome caused by stress is well described. Previous reports suggest that stress is known to caus e the release of endogenous substances such as catecholamine, beta-end orphine, 5-hydroxytryptamine, corticotropin-releasing factor, and thyr otropin-releasing hormone (TRH). However, the role played by these neu rohormonal mediators in bowel dysfunction under stress conditions is n ot well known. We investigated the influence of water-immersion stress or TRH administration on the expression of 60-kDa, 72-kDa, and 90-kDa heat-shock proteins (HSP60, HSP72, and HSP90, respectively) in rat sm all intestinal mucosa by Western blot and immunohistochemical analyses . The cytoprotective function of preinduced HSPs on experimentally ind uced mucosal damage also was studied. In order to investigate the infl uence of preinduction of HSP60 on small intestinal damage, the small i ntestinal lumen was perfused with 1.5% acetic acid 1 ml/min for 15 min with or without pretreatment with water-immersion stress or TRH admin istration. Expression of HSP60 was significantly increased by water-im mersion stress or TRH administration in the small intestinal mucosa, w hereas HSP72 and HSP90 did not increase. Interestingly, expression of this protein showed the biphasic peak pattern after water-immersion st ress or TRH administration. Each peak was observed 3-6 hr and 21-24 hr after the initiation of water-immersion stress or TRH administration. Immunohistochemical study also showed a significant increment of HSP6 0 in both the cytoplasm and nuclei of the small intestinal mucosal cel ls. No histopathologic alteration was observed in rat small intestinal mucosa after each treatment. Small intestinal damage caused by 1.5% a cetic acid perfusion was not influenced by preinduction of HSP60. We d emonstrated that water-immersion stress or TRH administration specific ally induced HSP60, although preinduction of this protein did not show a cytoprotective function in the small intestinal mucosa.