Role of α7nAChR in postoperative cognitive dysfunction in aged rats with tibial fracture / 中华麻醉学杂志

ABSTRACT

Objective To evaluate the role of α7 nicotinic acetylcholine receptor (α7nAChR) in postoperative cognitive dysfunction in aged rats with tibial fracture. Methods One hundred and fifty clean-grade healthy male Sprague-Dawley rats, aged 18-22 months, weighing 440-580 g, were divided into 5 groups ( n=30 each ) using a random number table method: control group ( group C ) , sham operation group ( group S) , tibial fracture group ( group T) , normal saline group ( group N) and α7nAChR agonist PUN282987 group (group P). Group C received no treatment. Ten percent chloral hydrate 0. 4 ml/100 g was injected intraperitoneally in group S. Group T underwent tibial fracture. PUN2829872. 4 mg/kg was in-traperitoneally injected at 5 min before tibial fracture in group P . The equal volume of normal saline was giv-en at 5 min before tibial fracture in group N. Morris water maze test was performed at day 7 after surgery. At days 1, 3 and 7 after surgery, the pathological changes of the hippocampal CA3 region were observed by haematoxylin and eosin staining, and the expression of α7nAChR, choline acetyltransferase ( ChAT ) , tumor necrosis factor-α( TNF-α) and interleukin-1β( IL-1β) in the hippocampal CA3 region was measured by Western blot. Results Compared with group C, the postoperative escape latency and swimming dis-tance were significantly prolonged, and the expression of α7nAChR, ChAT, TNF-α and IL-1β was up-regulated at each time point after operation in T, N and P groups ( P＜0. 05) , and no significant change was found in the parameters mentioned above in group S ( P＞0. 05) . Compared with group T, the postoper-ative escape latency and swimming distance were significantly shortened, and the expression of α7nAChR and ChAT was up-regulated and the expression of TNF-α and IL-1β was down-regulated at each time point after operation in group P ( P＜0. 05) , no significant change was found in the parameters mentioned above in group N ( P＞0. 05) , and the pathological changes of the hippocampal CA3 region were significantly at-tenuated in group P. Conclusion α7nAChR antagonism is involved in the development of postoperative cognitive dysfunction in aged rats with tibial fracture.