山东医药2023，Vol.63Issue(29)：7-10,4.DOI:10.3969/j.issn.1002-266X.2023.29.002
敲低S100A9对大鼠脑缺血再灌注损伤、炎症反应的影响及其机制
Effects of S100A9 knockdown on cerebral I/R injury and inflammation in rats and the mechanism
摘要
Abstract
Objective To investigate the effects of S100A9 knockdown on cerebral ischemia-reperfusion(I/R)inju-ry and inflammation in rats and to explore the related mechanism.Methods SD rats were randomly divided into the sham operation group,model group,Lsh-NC group,and Lsh-S100A9 group,respectively.The middle cerebral artery oc-clusion(MCAO)models were prepared by intraluminal suture method in the model group,Lsh-NC group,and Lsh-S100A9 group;the rats in the sham operation group only received the carotid artery exposure and wire embedding;in the Lsh-S100A9 group and Lsh-NC group,rats received S100A9 knockdown lentivirus or empty vector intracerebral injection at 24 h after modeling.RT-qPCR was used to detect S100A9 mRNA expression in the brain tissues of rats;neurological se-verity score(NSS)score was used to evaluate the degree of neurological impairment;infarct volume of brain tissue was measured by 2,3,5-triphenyltetrazolium chloride(TTC)staining;and IL-1β,IL-6 and tumor necrosis factor-α(TNF-α)were detected by ELISA.The protein expression levels of p65,phosphorylated p65(p-p65)and MyD88 in the brain tis-sues of rats in the Lsh-NC group and Lsh-S100A9 group were detected by Western blotting.Results S100A9 mRNA ex-pression level was as follows:the model group,Lsh-NC group>sham operation group>Lsh-S100A9 group;the neurologi-cal impairment score,ischemic cerebral infarction volume and IL-1β,IL-6,TNF-α expression levels in the brain tissues were in the following order:the model group,Lsh-NC group>Lsh-S100A9 group>sham operation group(both P<0.05).The expression levels of p-p65 and MyD88 protein in the Lsh-S100A9 group were lower than those in the Lsh-NC group(all P<0.01).Conclusion S100A9 knockdown can alleviate the cerebral I/R injury and inhibit brain inflammation in MCAO rats.The mechanism may be related to the regulation of NF-κB signaling pathway to affect the inflammatory re-sponse.关键词
S100A9/神经功能/脑梗死体积/炎症反应/NF-κB信号通路/脑缺血再灌注损伤Key words
S100A9/neurological function/brain infarct volume/inflammatory response/NF-κB signaling path-way/cerebral ischemia-reperfusion injury分类
医药卫生引用本文复制引用
杨越,潘燕,丛丽娜,白杨..敲低S100A9对大鼠脑缺血再灌注损伤、炎症反应的影响及其机制[J].山东医药,2023,63(29):7-10,4.基金项目
新疆维吾尔自治区自然科学基金项目(2022D01C574). （2022D01C574）
