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目的:观察蓝布正对局灶脑缺血大鼠梗死灶周围大脑皮质神经元凋亡及蛋白表达的影响,探讨其促脑卒中后神经功能恢复作用及机制。方法:72只SD大鼠采用线栓法建立脑缺血损伤模型(p MCAO),随机分成假手术组,模型组,蓝布正高、中、低剂量组(7.00,3.50,1.75 g·kg-1),银杏叶片组(0.007 g·kg-1),连续ig给药3 d。进行神经功能评分,四氮唑红(TTC)染色观察大鼠的脑梗死范围,苏木素-伊红(HE)染色观察梗死灶周围大脑皮质的病理形态学改变,原位细胞凋亡检测(TUNEL)梗死灶周围大脑皮质神经元凋亡,免疫组化检测梗死灶周围大脑皮质中B细胞淋巴瘤/白血病-2(Bcl-2)和Bcl-2相关X蛋白(Bax)蛋白表达的情况。结果:模型组一侧大脑中动脉永久性栓塞3 d大鼠神经功能评分增加,脑梗死范围增多,梗死灶周围大脑皮质部分神经元变性,Bcl-2蛋白表达下降,Bax蛋白水平升高,与假手术组比较,差异具有统计学意义(P<0.01);与模型组比较,蓝布正高、中、低剂量组均能不同程度减少神经功能评分,缩小脑梗死范围,改善梗死灶周围大脑皮质的病理形态学改变;抑制梗死灶周围大脑皮质神经元凋亡,促进抗凋亡蛋白Bcl-2的表达,抑制促凋亡蛋白Bax表达(P<0.05)。结论:蓝布正对大鼠脑缺血性损伤具有一定的保护作用,机制可能与其促进梗死灶周围大脑皮质Bcl-2水平增加,抑制Bax活性,提高脑组织抗缺血损伤的能力和抑制神经细胞凋亡有关。
OBJECTIVE: To observe the effect of Lvbuzheng on neuronal apoptosis and protein expression in cerebral cortex around focal infarction in focal cerebral ischemia rats, and to explore the mechanism and mechanism of Lvbuzheng on neurological recovery after stroke. Methods: Seventy-two Sprague-Dawley rats were randomly divided into sham-operation group, model group, positive control group, middle-dose and low-dose group 1), ginkgo leaf group (0.007 g · kg-1), continuous ig administration for 3 d. The neurological function score, TTC staining were used to observe the range of cerebral infarction in rats. The pathological changes of cerebral cortex around the infarct were observed by hematoxylin and eosin (HE) staining. TUNEL, The apoptosis of cerebral cortex neurons around the infarct area was detected by immunohistochemistry. The expressions of Bcl-2 and Bcl-2 in the cerebral cortex around the infarct area were detected by immunohistochemistry. Results: In the model group, on the 3rd day after permanent embolization of the middle cerebral artery, the neurological function score increased, the range of cerebral infarction increased, the degeneration of neurons in the cerebral cortex around the infarct area decreased, the expression of Bcl-2 protein decreased and the protein level of Bax increased Compared with sham-operation group, the difference was statistically significant (P <0.01). Compared with the model group, the positive, middle and low-dose groups were able to reduce the neurological score, reduce the range of cerebral infarction and improve the cerebral cortex (P <0.05) .At the same time, the apoptosis of cerebral cortex neurons in the infarcted area was inhibited, the expression of anti-apoptotic protein Bcl-2 was inhibited, and the expression of Bax protein was also inhibited (P <0.05). CONCLUSION: The blue cloth is protective against cerebral ischemic injury in rats. The mechanism may be related to the increase of Bcl-2 level, the inhibition of Bax activity, the ability of anti-ischemic injury and the inhibition of nerve function in cerebral cortex Apoptosis related.