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Background/AimsEthanol administration causes intestinal epithelial cell damage by increasing intestinal permeability and the translocation of endotoxins from intestinal bacterial flora. Heat shock proteins (HSPs) are associated with recovery and protection from cell damage. The aim of the current study was to investigate differences in the expression of HSPs in the small intestine and the biochemical changes attributable to ethanol-induced intestinal damage.MethodsEthanol (20%) was injected intraperitoneally (2.75 g/kg, 5.5 g/kg, 8.25 g/kg) in ICR mice and the same volume of saline was administered to controls. After 1 hour, the proximal, middle, and distal segments were taken from the small intestine and the degree of damage was analyzed. In each segment, the expression of HSPs was analyzed by western blotting. The expression of inflammatory mediators including interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), cyclooxygenase-2 (COX-2), and antioxidant enzyme such as glutathione-S-transferase were compared using real-time polymerase chain reaction assays.ResultsIn the control group, HSP70 increased in all segments of small intestine. Additionally, increases in the expression of HSP40 and HSP90 in the distal regions and an increase in HSP32 in the middle regions were observed. After ethanol treatment, greater histological damage was observed in the distal small intestine and significant decreases in HSPs were observed generally. Increased expression of IL-1β, TNF-α, and COX-2 was observed in small intestinal tissues exposed to ethanol-induced damage. However, there was no significant difference in the expression of an antioxidant enzyme.ConclusionsSignificant differences in the expression of HSPs in different intestinal regions were observed. These differences may have been attributable to the distribution of intestinal bacteria.

Background/Aims: In addition to the inhibition of cyclooxygenase-2, the chemopreventive effect of non-steroidal anti-inflammatory drugs on the nuclear translocation of β-catenin has been suggested in patients with familial adenoma polyposis. We investigated the effect of aspirin on the β-catenin signaling pathway in patients with sporadic colorectal adenoma. Methods: We selected patients diagnosed with colorectal adenoma. Patients who had been taking aspirin for more than 12 months were identified as the aspirin group, and those who did not were the non-aspirin group. Their characteristics, including size and degree of dysplasia, were compared. Immunohistochemical staining was conducted and the expression levels of nuclear β-catenin and cyclin D1 were investigated. Results: The median duration of aspirin intake was 37 months; there were no significant differences in the size, histological type, and degree of dysplasia between the two groups. Nuclear β-catenin expression was observed in 43.2% of the patients in the aspirin group and in 18.9% of those in the non-aspirin group (P < 0.05). There was no significant difference in nuclear cyclin D1 staining between the aspirin (78.4%) and non-aspirin (91.9%) groups. Conclusions: In this retrospective study, nuclear β-catenin expression in sporadic colorectal adenoma in the aspirin group was not inhibited compared with that in the non-aspirin group. Therefore, further prospective studies with a large number of patients are necessary. [ABSTRACT FROM AUTHOR]