Mechanism of α7nAChR agonist-induced protection in intestine in rats undergoing cardiopulmonary bypass: relationship with activity of enteric glial cells / 中华麻醉学杂志

ABSTRACT

Objective:To evaluate the mechanism of α7 nicotinic acetylcholine receptor (α7nAChR) agonist-induced protection of the intestine in rats undergoing cardiopulmonary bypass (CPB) and the relationship with the activity of enteric glial cells (EGCs).Methods:Seventy-two clean-grade adult male Sprague-Dawley rats, aged 400-500 g, were divided into 3 groups ( n=24 each) using a random number table method: sham operation group (group S), CPB group (group C) and α7nAChR agonist PHA568487 plus CPB group (group P). In group P, PHA568487 0.8 mg/kg was intraperitoneally injected, and 30 min later CPB model was established.At the beginning of CPB (T 0), at 1 h of CPB (T 1), and at 2 and 6 h after termination of CPB (T 2, 3), the rats were sacrificed, and intestinal tissues were obtained for examination of the pathological changes and for determination of the expression of ZO-1, occludin, glial fibrillary acidic protein (GFAP), and calcium-binding protein (S-100β protein) by Western blot.The immunohistochemical method was used to observe the positive expression of GFAP at T 2. Results:Compared with group S, the expression of GFAP and S-100β protein was significantly up-regulated, and the expression of ZO-1 and occludin was down-regulated at T 1-3( P<0.05), the positive expression of GFAP was increased, and the intestinal tissue injury was accentuated in C and P groups.Compared with group C, the expression of GFAP, ZO-1 and occludin was significantly up-regulated, and the expression of S-100β protein was down-regulated at T 1-3( P<0.05), the positive expression of GFAP was increased, and the intestinal tissue injury was reduced in group P. Conclusion:The mechanism by which α7nAChR agonist attenuates intestinal injury may be related to activating EGCs and improving intestinal barrier function in rats undergoing CPB.