XingNaoJing injections protect against cerebral ischemia/reperfusion injury and alleviate blood-brain barrier disruption in rats, through an underlying mechanism of NLRP3 inflammasomes suppression

查看全文 作　　者：QU Xiao-[1]Yu;ZHANG Yue-[1]Ming;TAO Li-[1]Na;GAO [1]Huan;ZHAI Jing-[1]Hui;SUN Jing-[1]Meng;SONG Yan-[1]Qing;ZHANG Si-[1]Xi

机构地区：[1]Department of Pharmacy, the First Hospital of Jilin University

出　　处：《Chinese Journal of Natural Medicines》索引2019年第17卷第7期,共8页

基　　金：surported by the National Natural Science Foundation of China(No.81803608);the Administration of Traditional Chinese Medicine of Jilin Province,China(No.2019133) 摘　　要：The aim of this study was to explore the neuroprotective effect and mechanism of XingNaoJing injections(XNJ) on cerebral ischemia injury and blood-brain barrier(BBB) disruption. Middle cerebral artery occlusion(MCAO) method was applicated to establish the model of cerebral ischemia/reperfusion(I/R) injury in rats. BBB permeability after I/R injury was assessed with the leaking amount of Evans Blue and the expression of occludin and ZO-1. The expression of NOD-like receptor family, pyrin domain containing(NLRP3) was checked to explore the inhibition of inflammation by XNJ. The results showed that XNJ could significantly increase the survival percent, decrease the infarct area and ameliorate neurological deficits and brain damage after I/R injury. Leaking amount of Evans Blue was reduced by XNJ, and the expression of tight junction protein, occludin and ZO-1 was also up-regulated by XNJ, which showed a role of protection on BBB disruption. The expression of NLRP3 was inhibited after exposure of XNJ, which was associated with inhibition of the inflammatory response. In summary, XNJ could suppress NLRP3 inflammasomes and improve BBB disruption and brain damage in rats after cerebral I/R injury, which provided a beneficial insight to further explore XNJ. 关键词：XINGNAOJING INJECTIONS Cerebral ISCHEMIA/REPERFUSION injury Blood-brain barrier NLRP3 INFLAMMASOMES

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XingNaoJing injections protect against cerebral ischemia/reperfusion injury and alleviate blood-brain barrier disruption in rats, through an underlying mechanism of NLRP3 inflammasomes suppression

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