黄角颗粒通过刺激PI3K/AKT/mTOR信号通路减轻脑缺血再灌注大鼠的脑损伤

Huangjiao granules ameliorate brain injury in rats with cerebral ischemia/reperfusion injury by stimulating PI3K/AKT/mTOR signaling pathway

目的探讨黄角颗粒对脑缺血再灌注损伤大鼠的作用及对磷脂酰肌醇3激酶/蛋白激酶B/哺乳动物雷帕霉素靶蛋白(PI3K/AKT/mTOR)信号通路的影响。方法采用线栓法构建大鼠脑缺血再灌注损伤模型,采用黄角颗粒进行处理。Zea Longa评分法进行大鼠神经功能评分、氯化三苯四唑(TTC)染色检测脑梗死百分比、HE染色观察脑组织病变情况、ELISA检测脑组织中白细胞介素10(IL-10)、IL-1β、肿瘤坏死因子α(TNF-α)含量,Western blot法检测PI3K、AKT、磷酸化的AKT(p-AKT)、mTOR和磷酸化的mTOR(p-mTOR)蛋白水平。结果黄角颗粒可显著减轻模型大鼠的神经功能缺损程度,减少脑梗死百分比,减轻脑组织病理损伤,显著上调脑组织中IL-10、PI3K、p-AKT和p-mTOR的水平,显著下调IL-1β和TNF-α的水平。结论黄角颗粒对脑缺血再灌注损伤的保护作用可能与促进PI3K/AKT/mTOR信号通路的激活相关。

Objective To investigate the protective effect of Huangjiao granules on rats with cerebral ischemia/reperfusion injury and the effect on phosphoinositide-3 kinase/protein kinase B/mammalian target of rapamycin（ PI3 K/AKT/mTOR）signaling pathway. Methods The rat models of cerebral ischemia/reperfusion injury were established by suture method and treated with Huangjiao granules. Zea Longa scoring was used to evaluate the neurological function of rats. The percentage of cerebral infarction was detected by triphenyl tetrazolium chloride（ TTC） staining. The pathological changes of brain tissues were observed by HE staining. The levels of interleukin 10（ IL-10）,IL-1β and tumor necrosis factor-α（ TNF-α） in the brain tissues were detected by ELISA. The expression levels of PI3 K, AKT, phosphorylated AKT（ p-AKT）, mTOR and phosphorylated mTOR（ p-mTOR） proteins were detected by Western blot analysis. Results Huangjiao granules could reduce the degree of neurological deficits, decrease the percentage of cerebral infarction, and lessen brain tissue pathological damage in the model rats. The expressions of IL-10,PI3 K,p-AKT and p-mTOR in the brain tissues of the model rats were significantly up-regulated by Huangjiao granules,but the expressions of IL-1β and TNF-α in the brain tissues of the model rats were significantly down-regulated by Huangjiao granules. Conclusion The protective effect of Huangjiao granules on rat models of cerebral ischemia/reperfusion injury may be related to the activation of PI3 K/AKT/mTOR signaling pathway.