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作 者:冯启锋 谷娟 孙红斌[2] Feng Qifeng;Gu Juan;Sun Hongbin(The Affiliated Traditional Chinese Medecine,Southwest Medical University,Luzhou,Sichuan 646000;Sichuan Province Pepole′s Hospital,Chengdu,Sichuan 610072,China.)
机构地区:[1]西南医科大学附属中医医院神经内科,四川泸州646000 [2]四川省医学科学院·四川省人民医院神经内科,四川成都610072
出 处:《四川医学》2021年第12期1194-1198,共5页Sichuan Medical Journal
摘 要:目的研究黄芩苷对氯化锂-匹罗卡品诱导的大鼠癫痫模型血脑屏障通透性的影响。方法将45只雄性SD大鼠随机分为空白对照组、癫痫模型组和黄芩苷干预组。采用氯化锂-匹罗卡品制备颞叶癫痫模型。运用伊文思蓝染色法评估血脑屏障的通透性,采用免疫组化及Western Blot确定紧密连接蛋白occludin的表达情况,ELISA检测评估炎症因子IL-1β和TNF-α的表达情况,电子显微镜观察血脑屏障超微结构变化。结果与模型组相比,黄芩苷延长了癫痫发作潜伏期,降低了发作级别,差异有统计学意义(P<0.05)。黄芩苷降低了脑组织中伊文思蓝的渗出,增加了occludin的表达,降低了IL-1β和TNF-α的表达水平,差异有统计学意义(P<0.05)。黄芩苷组血脑屏障超微结构的破坏得到明显改善。结论黄芩苷在氯化锂-匹罗卡品致痫模型中具有显著的血脑屏障保护作用,其机制可能与上调occludin的表达,减少炎症因子IL-1β和TNF-α的表达有关。Objective To study the effect of baicalin on the permeability of blood-brain barrier(BBB)in rats with epilepsy induced by lithium chloride-pilocarpine.Methods 45 male Sprague-Dawley rats were randomly divided into control group,epilepsy model group and baicalin intervention group.A model of temporal lobe epilepsy was prepared using lithium chloride-pilocarpine.The permeability of the BBB was assessed by Evans blue staining.The expression of tight junction protein occludin was determined by immunohistochemistry and western blot.The expression of inflammatory factors IL-1βand TNF-αwere assessed by ELISA.Ultrastructural changes of BBB were observed by electron microscope.Results Compared with the model group,baicalin extended the latency of epileptic seizures and deduced the grade of seizures(P<0.05).Baicalin reduced the exudation of Evans blue in brain tissues,increased the expression of occludin,and decreased the expression levels of IL-1βand TNF-α(P<0.05).The ultrastructural damage of BBB in baicalin group was significantly improved.Conclusion Baicalin has a significant protective effect on BBB in the model of epilepsy induced by lithium chloride-pilocarpine,and its mechanism may be related to up-regulating the expression of occludin and down-regulating the expression of inflammatory factors IL-1βand TNF-α.
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