目的 通過磷脂酰肌醇3-激酶（PI3K）/蛋白激酶B（Akt）信號通路探討牡荊素對腦外傷大鼠的神經(jīng)保護(hù)作用。方法 選用SD大鼠90只，隨機分成假手術(shù)組，模型組，牡荊素假手術(shù)組（12 mg/kg牡荊素），牡荊素低（3 mg/kg牡荊素）、高劑量組（12 mg/kg牡荊素）和吡拉西坦組（20 mg/kg吡拉西坦），每組18只。采用自由落體致傷法建立腦外傷大鼠模型；采用神經(jīng)功能評分法評價神經(jīng)功能缺損程度；測定腦組織的含水量；蘇木素伊紅（HE）染色檢測腦組織病理變化；TUNEL法檢測腦組織神經(jīng)細(xì)胞的凋亡情況；ELISA法檢測腦組織丙二醛（MDA）、超氧化物歧化酶（SOD）、谷胱甘肽過氧化物酶（GSH-Px）水平；Western blotting法檢測腦組織中PI3K、p-PI3K、Akt、p-Akt、mTOR、p-mTOR蛋白水平。結(jié)果 與假手術(shù)組相比，模型組大鼠神經(jīng)元變性壞死，毛細(xì)血管破裂，可見大量出血、炎性細(xì)胞浸潤，神經(jīng)功能受損評分、細(xì)胞凋亡指數(shù)、腦組織含水量及MDA含量顯著升高（P<0.05），SOD、GSH-Px含量及p-PI3K、p-Akt、p-mTOR蛋白水平顯著降低（P<0.05）。與模型組相比，牡荊素低、高劑量組和吡拉西坦組大鼠病理變化均有一定程度減輕，神經(jīng)功能受損評分、細(xì)胞凋亡指數(shù)、腦組織含水量及MDA含量顯著降低（P<0.05），SOD、GSH-Px含量及p-PI3K、p-Akt、p-mTOR蛋白水平均顯著升高（P<0.05）。假手術(shù)組和牡荊素假手術(shù)組各項指標(biāo)差異無統(tǒng)計學(xué)意義。牡荊素高劑量組和吡拉西坦組各項指標(biāo)差異無統(tǒng)計學(xué)意義。結(jié)論 牡荊素可能通過激活PI3K/Akt信號通路，發(fā)揮腦外傷大鼠的神經(jīng)保護(hù)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.

R965

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