CAJ | 학술논문

目的：评价全脑缺血再灌注损伤老龄大鼠海马胆碱能抗炎通路的变化。方法老龄雄性SD大鼠120只，18～22月龄，体重450～600 g ，采用随机数字表法，将其分为2组（ n＝60）：假手术组（S组）和全脑缺血再灌注组（I/R组）。I/R组采用四血管阻断法制备大鼠全脑缺血再灌注损伤模型。分别于再灌注1、3、5和7 d时处死15只大鼠，取脑组织，测定海马CA1区神经元凋亡率、α7烟碱型乙酰胆碱受体（α7nAChR）、胆碱乙酰基转移酶（ChAT）、TNF-α和IL-1β表达。结果与S组比较，I/R组再灌注不同时点海马组织神经元凋亡率升高，α7nAChR、ChAT、TNF-α和 IL-1β表达上调（ P＜0.05或0.01）；再灌注期间海马组织α7nAChR和ChAT表达逐渐上调，到再灌注5 d时达高峰（ P＜0.05）。结论全脑缺血再灌注损伤老龄大鼠海马胆碱能抗炎通路激活，该通路激活是抑制脑组织过度炎性反应的内源性机制。
목적：평개전뇌결혈재관주손상노령대서해마담감능항염통로적변화。방법노령웅성SD대서120지，18～22월령，체중450～600 g ，채용수궤수자표법，장기분위2조（ n＝60）：가수술조（S조）화전뇌결혈재관주조（I/R조）。I/R조채용사혈관조단법제비대서전뇌결혈재관주손상모형。분별우재관주1、3、5화7 d시처사15지대서，취뇌조직，측정해마CA1구신경원조망솔、α7연감형을선담감수체（α7nAChR）、담감을선기전이매（ChAT）、TNF-α화IL-1β표체。결과여S조비교，I/R조재관주불동시점해마조직신경원조망솔승고，α7nAChR、ChAT、TNF-α화 IL-1β표체상조（ P＜0.05혹0.01）；재관주기간해마조직α7nAChR화ChAT표체축점상조，도재관주5 d시체고봉（ P＜0.05）。결론전뇌결혈재관주손상노령대서해마담감능항염통로격활，해통로격활시억제뇌조직과도염성반응적내원성궤제。
Objective To evaluate the changes in cholinergic anti-inflammatory pathway in hippocampi global in aged rats with cerebral ischemia/reperfusion (I/R ) injury .Methods One hundred and twenty male Sprague-Dawley rats , aged 18-22 months ,weighing 450-600 g ,were randomly divided into 2 groups ( n= 60 each):sham operation group (group S) and global cerebral I/R group (group I/R) .The animals were anesthetized with intraperitoneal 10% chloral hydrate 0.4 ml/100 g .Global cerebral I/R was induced by 4-vessel occlusion method described by Pulsinelli .Fifteen rats were sacrificed at 1 ,3 ,5 and 7 days of reperfusion ,and brains were removed for determination of neuronal apoptosis and expression of α7 nicotinic acetylcholine receptor (α7nAChR ) , choline acetyltransferase (ChAT ) ,tumor necrosis factor-α(TNF-α) and interleukin-1β(IL-1β) in the hippocampal CA1 region .The apoptosis rate was calculated .Results Compared with group S ,the apoptosis rate was increased and the expression of α7nAChR ,ChAT ,TNF-αand IL-1βwas up-regulated in group I/R ( P<0.05 or 0.01 ) . The expression of α7nAChR and ChAT was up-regulated gradually during reperfusion and peaked at 5 day of reperfusion ( P< 0.05 ) .Conclusion Global cerebral I/R injury can activate cholinergic anti-inflammatory pathway in aged rat hippocampi ,and the activation of this pathway is the endogenous mechanism of inhibition of excessive inflammatory responses in brain tissues .