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目的探讨吗啡预处理对大鼠脑缺血-再灌注损伤后神经元凋亡、Bel-2及Bax蛋白表达的影响。方法 Wistar大鼠32只随机分成假手术组、模型组、吗啡1mg·kg~(-1)组、吗啡7mg·kg~(-1)组,各8只。四动脉阻断法建立脑缺血模型。缺血前60min腹腔注射给药,假手术组和模型组给予生理盐水。脑缺血8min、再灌注24h后取大鼠的脑组织,HE染色观察海马区脑组织病理学改变、TUNEL法检测神经元凋亡、免疫组化法观察Bcl-2及Bax蛋白表达。结果吗啡预处理使海马神经元病理改变减轻、凋亡细胞数及Bax表达减少(P<0.01),而Bcl-2表达增加(P<0.01);且吗啡7mg·kg~(-1)组减少神经元凋亡及改善神经元病理变化的作用更为显著(P<0.01)。结论吗啡预处理可减少缺血-再灌注损伤后神经元凋亡,其作用机制可能与其影响Bcl-2和Bax蛋白表达有关。吗啡7mg·kg~(-1)预处理的保护作用更为显著。
Objective To investigate the effect of morphine preconditioning on the neuronal apoptosis, Bel-2 and Bax protein expression after cerebral ischemia-reperfusion injury in rats. Methods Thirty - two Wistar rats were randomly divided into sham operation group, model group, morphine 1 mg · kg -1 group and morphine 7 mg · kg -1 group. Four-artery occlusion method was used to establish cerebral ischemia model. 60min before ischemia by intraperitoneal injection, sham operation group and model group given saline. Brain tissue was collected for 8 min after cerebral ischemia and 24 h after reperfusion. Pathological changes of hippocampus were observed by HE staining. Neuronal apoptosis was detected by TUNEL method. Bcl-2 and Bax protein expression was observed by immunohistochemistry. Results Morphine preconditioning could reduce the pathological changes of hippocampal neurons, decrease the number of apoptotic cells and the expression of Bax (P <0.01), and increase the expression of Bcl-2 (P <0.01), and decrease the levels of morphine 7 mg · kg -1 Neuronal apoptosis and pathological changes of neurons were more significant (P <0.01). Conclusion Morphine preconditioning can reduce neuronal apoptosis after ischemia-reperfusion injury and its mechanism may be related to its effect on Bcl-2 and Bax protein expression. The protective effect of morphine 7mg · kg -1 pretreatment was more significant.