论文部分内容阅读
目的探讨大鼠局灶性脑缺血再灌注后当归补血汤对大脑皮质神经元的保护作用。方法雄性SD大鼠48只随机分为假手术组、大脑中动脉阻塞再灌注组、生理盐水对照组、当归补血汤治疗组。治疗组术前连续6d灌胃,每日2次(早、晚各1次),术后4h再灌胃2次,每次2.5ml,次日取材。观察各组大鼠神经行为学缺陷;脑梗死体积和梗死率变化;血脑屏障通透性变化;大脑皮质神经元的形态和数量;大脑皮质神经元p53和天冬氨酸特异性半胱氨酸蛋白酶3(Caspase-3)的表达情况以及大脑皮质凋亡神经元的形态和数量。结果与缺血再灌注组、生理盐水对照组比较,当归补血汤治疗组2,3,5-氯化三苯四氮唑(TTC)染色显示大脑皮质梗死区体积减少(P<0.05);荧光显微镜观察脑组织中伊文斯蓝的含量减少(P<0.05),Nissl染色显示大脑皮质神经元数量增加(P<0.05);免疫组织化学方法显示大脑皮质神经元Caspase-3、p53的阳性细胞数减少(P<0.05);TUNEL染色法显示大脑皮质神经元凋亡细胞减少(P<0.05)。结论当归补血汤治疗组能减少大脑皮质神经元的死亡,这与其减少大脑皮质神经元Caspase-3、p53的表达,并通过减少细胞凋亡起保护作用有关。
Objective To investigate the protective effects of Danggui Buxue Tang on cerebral cortex neurons after focal cerebral ischemia-reperfusion in rats. Methods Forty-eight male Sprague-Dawley rats were randomly divided into sham-operation group, middle cerebral artery occlusion-reperfusion group, saline control group and Dangguibuxuetang group. The patients in the treatment group were given gavage for 6 days continuously, twice daily (morning and evening), and then re-gavaged twice a day for 4 hours. The neurobehavioral defects, cerebral infarction volume and infarct rate, changes of blood-brain barrier permeability, morphology and number of neurons in cerebral cortex were observed. The expressions of p53 and caspase-cysteine The expression of Caspase-3 and the morphology and quantity of apoptotic neurons in cerebral cortex. Results Compared with ischemia reperfusion group and saline control group, the volume of infarct zone in cerebral cortex was decreased by DTC treatment with Dangguibuxue decoction (P <0.05) The content of Evans blue in the brain tissue was reduced by microscope (P <0.05), and the number of neurons in the cerebral cortex was increased by Nissl staining (P <0.05). The number of positive cells of Caspase-3 and p53 in cerebral cortex neurons (P <0.05). The number of apoptotic neurons in cerebral cortex decreased with TUNEL staining (P <0.05). Conclusion Dangguibuxue Decoction can reduce the death of cerebral cortex neurons, which is related to the decrease of the expression of Caspase-3, p53 in cerebral cortex neurons and the decrease of apoptosis.