灯盏乙素对激活的小胶质细胞中PI3K表达和磷酸化水平的影响
The effects of scutellarin on P13K expression and phosphorylation level in activated microglia
杨丽芳 1段兆达 1杨毓甲 1徐冬垚 1吴春云 1杨力1
作者信息
- 1. 昆明医科大学基础医学院人体解剖与组织胚胎学系,昆明 650500
- 折叠
摘要
目的:探究灯盏乙素对激活的小胶质细胞磷脂酰肌醇3-激酶(P13K)和磷酸化PI3K(p-PI3K)水平的影响.方法:用大鼠大脑中动脉闭塞(MCAO)法制备脑缺血模型,大鼠随机分成假手术组(Sham)、脑缺血组(MCAO)、脑缺血+灯盏乙素组(MCAO+S).利用糖氧剥夺(OGD)法制备BV2小胶质细胞缺血缺氧损伤模型,随机分成对照组(Control)、OGD组、OGD+灯盏乙素组(OGD+S).运用免疫荧光双标染色和Western Blot法检测不同组中小胶质细胞PI3K及PI3K磷酸化水平的变化.结果:体内和体外免疫荧光及Western Blot结果均显示,激活的小胶质细胞中PI3K磷酸化水平明显增加(P<0.05),灯盏乙素干预后PI3K磷酸化水平进一步升高(P<0.05);PI3K在各组间无明显变化(P>0.05).结论:灯盏乙素可能通过上调激活的小胶质细胞中PI3K的磷酸化水平,对脑缺血发挥积极的治疗作用.
Abstract
Objective:To explore the impact of scutellarin on the levels of phosphatidylinositol 3-kinase(P13K)and phosphorylated P13K(p-PI3K)in activated microglia.Methods:A rat cerebral ischemia model was made by middle cerebral artery occlusion(MCAO)method.SD rats were randomly divided into three groups:sham operation group(Sham),cerebral ischemia group(MCAO),and cerebral ischemia with scutellarin group(MCAO+S).A model of ischemia-hypoxia injury of BV2 microglia was established by glucose-oxygen deprivation(OGD)and randomly assigned as control group(Control),OGD group and OGD+scutellarin group(OGD+S).Changes in PI3K and p-PI3K expres-sion in microglia were assessed using double immunofluorescence staining and Western Blot.Results:Immunofluores-cence staining and Western Blot analyses revealed a significant increase in p-PI3K levels in activated microglia both in vivo and in vitro(P<0.05).Furthermore,treatment with scutellarin led to a further elevation in p-PI3K(P<0.05).However,there were no significant alterations observed in PI3 K expression among the groups(P>0.05).Conclusion:Scutellarin may play a positive role in the treatment of cerebral ischemia by up-regulating the phosphorylation level of P13K in activated microglia.
关键词
脑缺血/灯盏乙素/小胶质细胞/磷脂酰肌醇3-激酶/大鼠Key words
cerebral ischemia/scutellarin/microglia/phosphatidylinositol 3-kinase(PI3K)/rat引用本文复制引用
基金项目
国家自然科学基金(81960223)
云南省科技厅昆医联合专项(202301AY070001-163)
出版年
2024