黄芪甲苷对脑缺血再灌注大鼠炎症因子及超微结构的影响

Effects of astragalosideⅣon inflammatory factors and ultrastructure in rats with cerebral ischemia reperfusion

目的观察黄芪甲苷对脑缺血再灌注大鼠炎症因子及超微结构的影响。方法以SD大鼠为实验对象,采用大脑中动脉闭塞(MCAO)法建立大鼠脑缺血再灌注损伤模型。将40只SD雄性大鼠,随机分为假手术组、模型组(脑缺血再灌注损伤组)、黄芪甲苷组和尼莫地平组(阳性药物组)。除假手术组之外,其余组脑缺血2 h后再灌注24 h,其中黄芪甲苷组和尼莫地平组于造模前一周腹腔注射给药。用Zea Longa评分法检测各组大鼠神经功能缺损情况;TTC染色检测脑梗死体积;ELISA法检测脑组织中炎症因子--肿瘤坏死因子α(TNF-α)、白细胞介素-6(IL-6)和白细胞介素-1β(IL-1β)的含量;尼氏染色检测大脑皮质区神经细胞损伤;透射电子显微镜检测大脑皮质区神经细胞超微结构变化。结果假手术组大鼠神经功能正常,未见脑梗死病灶,神经细胞和尼氏体数量丰富,细胞排列整齐,细胞超微结构清晰正常;与假手术组相比,模型组大鼠神经功能缺损较为严重,脑梗死体积显著增加(P<0.05),炎症因子TNF-α、IL-6、IL-1β含量均升高(P<0.05),细胞排列混乱,细胞核变形、固缩,染色质分布不均匀;与模型组比,黄芪甲苷组和尼莫地平组大鼠神经功能均得到改善,脑梗死体积均减少(P<0.05),TNF-α、IL-6、IL-1β含量均显著下降(P<0.05),细胞排列较为整齐,细胞核规整,染色质分布较为均匀。结论黄芪甲苷可抑制大鼠脑缺血再灌注损伤,改善神经细胞超微结构变化,其作用机制可能与黄芪甲苷减轻炎症反应有关。

Objective To observe the effect of astragalosideⅣon inflammatory factors and ultrastructure in rats with cerebral ischemia reperfusion.Methods A cerebral ischemia reperfusion injury model was established in SpragueDawley(SD)rats by middle cerebral artery occlusion.Forty male SD rats were randomly divided into a sham operation group,model group(cerebral ischemia reperfusion injury group),astragalosideⅣgroup and nimodipine group(positive drug group).All groups except the sham operation group were reperfused for 24 hours after 2 hours of cerebral ischemia.In the treatment groups,astragalosideⅣand nimodipine were respectively injected intraperitoneally one week before model establishment.The Zea Longa scoring method was used to detect neurological deficits of rats in each group.TTC staining was used to detect the volume of cerebral infarction.The ELISA method was used to detect the inflammatory factor levels in brain tissue,including tumor necrosis factoR-α(TNF-α),interleukin-6(IL-6)and interleukin-1β(IL-1β).Nissl staining was used to observe neuronal damage in the cerebral cortex.Transmission electron microscopy was used to observe the ultrastructural changes of neurons in the cerebral cortex.Results In the sham operation group,no neurological deficits or cerebral infarction was observed,and abundant nerve cells and Nissl bodies were present.The cells were arranged neatly,and the ultrastructure was clear and normal.Compared with the sham operation group,neurological impairment was more serious in the model group.The cerebral infarction volume was significantly increased(P<0.05).The inflammatory factor content(TNF-α,IL-6 and IL-1β)was increased(P<0.05).The cells had a disorderly arrangement,the nuclei were deformed and showed pyknosis,and the chromatin was unevenly distributed.Compared with the model group,the neurological function of rats in astragalosideⅣand nimodipine groups was improved,the cerebral infarction volume was decreased(P<0.05),the TNF-α,IL-6 and IL-1βcontent was significantly decreased(P<0.05),the cell arrangement was more orderly,the cell nucleus was regular,and the chromatin distribution was more uniform.Conclusions AstragalosideⅣcan inhibit cerebral ischemia reperfusion injury and improve the ultrastructural changes of nerve cells in rats.Its mechanism may be related to alleviation of the inflammatory reaction.