摘要
目的观察梗死后高迁移率族蛋白B1(HMGB1);晚期糖基化终产物(RAGE);Toll样受体4(TLR4);核因子-κB(NF-κB);紧密连接蛋白5(claudin-5)的表达变化,并观察行为学评分、脑水肿及梗死体积,探讨甘草甜素(Gly)对脑缺血的保护机制。方法线栓法制备大鼠大脑中动脉永久性闭塞(pMCAO)模型。Gly进行干预,比较各组之间神经功能缺损评分、患侧脑水肿和脑梗死体积的变化。同时用免疫组化、实时定量PCR和Western blot方法,分别在梗死后24 h观察HMGB1、RAGE、TLR4、NF-κB和claudin-5蛋白表达变化,以及TLR4、NF-κB和claudin-5的基因表达变化。结果 Gly显著改善神经功能缺失,减轻梗死后患侧脑水肿,减小脑梗死体积(P<0.05);Gly能明显降低HMGB1、RAGE、TLR4和NF-κB的表达(P<0.05),升高claudin-5的表达(P<0.05)。结论 Gly对缺血性脑组织发挥保护作用可能是通过下调HMGB1、RAGE、TLR4、NF-κB的表达,升高claudin-5的表达实现的。
Objective To observe the expressions of HMGB1/RAGE/TLR4/NF-κB/claudin-5 and to evaluate the underling mechanisms of glycyrrhizin(Gly). Method Male Sprague-Dawley rats were sufferedfrom permanent middle cerebral occlusion( pMCAO). Gly was systemically administered to detect the impact on HMGB1, RAGE, TLR4, NF-κB and claudin-5 at 24 h after cerebral infarction by immunohistochemical, western blot and qRT-PCR. The neurological deficits, brain water content and infarct volume were detected. Results Gly dramatically alleviated neurological deficit, restrained edema and reduced infarct volume( P<0.05). Simultaneously, degraded the expression of HMGB1, RAGE, TLR4 and NF-κB and upgraded the expression of claudin-5( P<0.05). Conclusion Gly protected the cerebral from the injury caused by pMCAO, and this role may be through upregulation of claudin-5 and downregulation of HMGB1, RAGE, TLR4 and NF-κB.
作者
乔会敏
陈林玉
杜媛媛
张祥建
李震中
Qiao Huimin;Chen Linyu;Du Yuanyuan;Zhang Xiangjian;Li Zhenzhong(Department of Neurology,the Second Hospital of Hebei Medical University,Shijiazhuang 050000,China)
出处
《脑与神经疾病杂志》
2019年第5期287-292,共6页
Journal of Brain and Nervous Diseases
基金
国家自然科学基金项目(81571292)
