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目的观察步长脑心通对大鼠局灶性脑缺血再灌注损伤的保护作用及其机制。方法采用线栓法建立SD大鼠大脑中动脉阻塞(MCAO)再灌注模型,随机将30只大鼠分为假手术组、对照组、脑心通治疗组各10只,采用神经功能缺损评分对大鼠神经功能缺损程度进行评价,采用免疫组化和Westernblot分别检测CD68、白细胞介素1β(IL-1β)的表达差异,并通过TUNEL、尼氏染色检测大鼠神经细胞的凋亡。结果脑心通治疗组CD68、TUNEL、尼氏阳性细胞数及IL-1β的表达均较对照组明显减少(P<0.05),差异具有统计学意义。结论脑心通能够明显减轻缺血再灌注损伤中脑组织的损伤程度,降低神经细胞的凋亡,其作用机制可能是通过抑制小胶质细胞激活导致的炎症介质释放,进而阻断缺血神经细胞的凋亡。
Objective To observe the protective effect and mechanism of naohuan naoxintong on focal cerebral ischemia-reperfusion injury in rats. Methods The model of middle cerebral artery occlusion (MCAO) reperfusion in SD rats was established by thread occlusion. Thirty rats were randomly divided into sham-operated group, control group and Naoxintong group. Each group was given neurological deficit score The degree of neurological deficit in rats was evaluated. The expressions of CD68 and IL-1β were detected by immunohistochemistry and Western blot respectively. The apoptosis of neurons was detected by TUNEL and Nissl staining. Results The expression of CD68, TUNEL, NIH positive cells and IL-1β in Naoxintong treatment group were significantly lower than those in control group (P <0.05), and the difference was statistically significant. Conclusion Naoxintong can obviously reduce the damage of brain tissue in ischemia-reperfusion injury and decrease the apoptosis of nerve cells. Its mechanism may be through inhibiting the release of inflammatory mediators caused by microglial activation and then blocking the ischemic nerve Apoptosis of cells.