Expression of Heat Shock Proteins and Cytokines in Response to Ethanol Induced Damage in the Small Intestine of ICR Mice.
- Author:
Sung Won LEE
1
;
Dong Wook CHOI
;
Sung Chul PARK
;
Hee Jung KIM
;
Yang Hoon NAM
;
Dae Hee CHOI
;
Chang Don KANG
;
Sung Joon LEE
;
Wan Joo CHUN
;
Young Joon RYU
Author Information
- Publication Type:Original Article
- Keywords: Intestine, small; Heat shock protein; Ethanol
- MeSH: Animals; Bacteria; Blotting, Western; Cyclooxygenase 2; Cytokines*; Endotoxins; Epithelial Cells; Ethanol*; Heat-Shock Proteins*; Interleukin-1beta; Intestine, Small*; Mice; Mice, Inbred ICR*; Permeability; Real-Time Polymerase Chain Reaction; Tumor Necrosis Factor-alpha
- From:Intestinal Research 2014;12(3):205-213
- CountryRepublic of Korea
- Language:English
- Abstract: BACKGROUND/AIMS: Ethanol 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. METHODS: Ethanol (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-1beta (IL-1beta), tumor necrosis factor-alpha (TNF-alpha), cyclooxygenase-2 (COX-2), and antioxidant enzyme such as glutathione-S-transferase were compared using real-time polymerase chain reaction assays. RESULTS: In 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-1beta, TNF-alpha, 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. CONCLUSIONS: Significant differences in the expression of HSPs in different intestinal regions were observed. These differences may have been attributable to the distribution of intestinal bacteria.
