目的 通过磷脂酰肌醇3-激酶（PI3K）/蛋白激酶B（Akt）信号通路探讨牡荆素对脑外伤大鼠的神经保护作用。方法 选用SD大鼠90只，随机分成假手术组，模型组，牡荆素假手术组（12 mg/kg牡荆素），牡荆素低（3 mg/kg牡荆素）、高剂量组（12 mg/kg牡荆素）和吡拉西坦组（20 mg/kg吡拉西坦），每组18只。采用自由落体致伤法建立脑外伤大鼠模型；采用神经功能评分法评价神经功能缺损程度；测定脑组织的含水量；苏木素伊红（HE）染色检测脑组织病理变化；TUNEL法检测脑组织神经细胞的凋亡情况；ELISA法检测脑组织丙二醛（MDA）、超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH-Px）水平；Western blotting法检测脑组织中PI3K、p-PI3K、Akt、p-Akt、mTOR、p-mTOR蛋白水平。结果 与假手术组相比，模型组大鼠神经元变性坏死，毛细血管破裂，可见大量出血、炎性细胞浸润，神经功能受损评分、细胞凋亡指数、脑组织含水量及MDA含量显著升高（P<0.05），SOD、GSH-Px含量及p-PI3K、p-Akt、p-mTOR蛋白水平显著降低（P<0.05）。与模型组相比，牡荆素低、高剂量组和吡拉西坦组大鼠病理变化均有一定程度减轻，神经功能受损评分、细胞凋亡指数、脑组织含水量及MDA含量显著降低（P<0.05），SOD、GSH-Px含量及p-PI3K、p-Akt、p-mTOR蛋白水平均显著升高（P<0.05）。假手术组和牡荆素假手术组各项指标差异无统计学意义。牡荆素高剂量组和吡拉西坦组各项指标差异无统计学意义。结论 牡荆素可能通过激活PI3K/Akt信号通路，发挥脑外伤大鼠的神经保护作用。
Objective To investigate the neuroprotective effect of vitexin on traumatic brain injury in rats through phosphatidylinositol 3-kinase (PI3K)/ protein kinase B (Akt) signaling pathway. Methods The rat model of brain injury was established by free falling body injury. Ninety SD rats were randomly divided into mock surgical group, model group, low dose vitexin group (3 mg/kg vitexin), high dose vitexin group (12 mg/kg vitexin), piracetam group（20 mg/kg piracetam）and vitexin mock surgical group (12 mg/kg vitexin), with eighteen rats in each group. Neurological function score was used to evaluate the degree of neurological deficit; the water content of brain tissue was measured; hematoxylin eosin (HE) staining was used to detect the pathological changes of brain tissue; TUNEL method was used to detect the apoptosis of nerve cells in brain tissue; the levels of MDA, SOD and GSH-Px were detected by ELISA; the protein levels of PI3K, p-PI3K, Akt, p-Akt, mTOR and p-mTOR were detected by Western blotting. Results Compared with those in the sham operation group, neurons in the model group were degenerated and necrotic, and the capillaries were ruptured, massive hemorrhage and inflammatory cell infiltration were observed in the model group, the neurological impairment score, apoptosis index, brain water content and MDA content were significantly higher(P<0.05), the contents of SOD and GSH-Px, the protein levels of p-PI3K, p-Akt and p-mTOR were significantly lower (P<0.05). Compared with those in the model group, the pathological changes in the low and high dose vitexin groups and piracetam groups were alleviated to some extent, the neurological impairment score, apoptosis index, brain water content and MDA content were significantly lower (P<0.05), the contents of SOD and GSH-Px, the protein levels of p-PI3K, p-Akt and p-mTOR were significantly higher (P<0.05). There was no significant difference between the mock surgical group and the vitexin sham operation group. And there was no significant difference between the high dose vitexin group and piracetam group. Conclusion Vitexin may play a neuroprotective role in traumatic brain injury rats by activating PI3K/Akt signaling pathway.