黄芩苷通过调控PI3K/AKT/NF-κB通路改善大鼠脑出血后的神经元凋亡

Baicalin alleviate neuronal apoptosis by regulating PI3K/AKT/NF-κB signaling pathway after intracerebral hemorrhage in rats

目的研究黄芩苷(Bai)对脑出血模型大鼠神经元凋亡的改善作用并探讨其作用机制。方法选取30只健康雄性Sprague-Dawley大鼠随机分为假手术组(Sham)、脑出血组(ICH)、黄芩苷治疗组(Bai),通过胶原酶IV注射法构建大鼠ICH模型。进行神经功能评分;测定各组大鼠脑组织含水量;HE染色检测脑组织形态;TUNEL法检测大鼠神经元凋亡数量;Western blot方法检测BAX、Bcl-2、Caspase-3以及PI3K/AKT/NF-κB信号通路相关蛋白的表达。结果黄芩苷能够降低ICH大鼠神经功能评分、减轻ICH模型大鼠的脑水肿、降低ICH大鼠凋亡神经元的数量、上调Bcl-2/Bax比率、降低Cleved-Caspase-3的表达水平、激活PI3K/AKT信号抑制NF-κB蛋白的表达。结论Bai可通过调控PI3K/AKT/NF-κB信号通路改善ICH大鼠神经元的凋亡,从而减轻ICH大鼠的脑水肿、改善其神经功能。

Objective To investigate the therapeutic effect and mechanism of Baicalin(Bai)on neuronal apoptosis in a rat model of intracerebral hemorrhage(ICH).Methods 30 healthy male Sprague-Dawley(SD)rats were randomly assigned into sham group(Sham group),intracerebral hemorrhage model group(ICH group),Baicalin group(Bai group).ICH model was established by collagenase IV injection.The neurological deficits were evaluated and water content of the brain tissue was examined.HE staining was performed to assessed histological morphology.TUNEL was used to detect the number of positive apoptotic cells.Western blot was used to detect the expression of BAX,Bcl-2,Caspase-3 and PI3K/AKT/NF-κB signaling pathway-related proteins.Results Baicalin can reduce the neural function score of ICH rats,reduce the cerebral edema of ICH model rats,reduce the number of apoptotic neurons in ICH rats,up-regulate the ratio of Bcl-2/Bax,reduce the expression of Cleved-Caspase-3,activate PI3K/AKT signal and inhibit the expression of NF-κB.Conclusion Baicalin can improve the apoptosis of ICH rat neurons by regulating PI3K/AKT/NF-κB signaling pathway,thus alleviating brain edema and improving neural function in ICH rats.