摘要
目的 探究长托宁预处理对内毒素诱导脑损伤大鼠的神经保护作用及可能机制。方法 SD大鼠随机分为对照组(Control)、内毒素诱导脑损伤大鼠模型组(LPS)、长托宁预处理组(PH),每组10只。观察经长托宁预处理后大鼠脑损伤情况,ELISA方法检测炎症因子和氧化应激因子含量;TUNEL检测细胞凋亡;Real-time PCR检测LncRNA-HOTAIR表达;Western blot检测p-NF-κB p65、NF-κB p65蛋白表达。结果 长托宁减轻内毒素诱导大鼠脑损伤,抑制炎性反应,提高SOD、GSH-Px活性,降低MDA水平,下调LncRNAHOTAIR基因表达以及p-NF-κB p65磷酸化水平。结论 长托宁抑制内毒素诱导脑损伤大鼠炎症反应,与下调LncRNA-HOTAIR表达,抑制NF-κB活性相关。
Objective To explore the neuroprotective effect and its mechanism of penehyclidine hydrochloride pretreatment on endotoxin-induced brain injury in rats. Methods SD rats were randomly divided into control, endotoxininduced brain injury model(LPS), and penehyclidine hydrochloride group(PH), 10 rats in each group. The contents of inflammatory factors and oxidative stress factors were determined by ELISA. Cell apoptosis was detected by TUNEL.Expression of lncRNA-HOTAIR was detected by real-time PCR. The expression of p-NF-κB p65 and NF-κB p65protein was detected by Western blot. Results Penehyclidine hydrochloride alleviated endotoxin-induced brain damage,inhibited inflammatory response, increased the activity of SOD and GSH-Px, and reduced the level of MDA, down-regulated the level of lncRNA-HOTAIR and p-NF-κB p65. Conclusion Penehyclidine hydrochloride inhibits endotoxin-induced inflammation response, which is related to the downregulation of lncRNA-HOTAIR expression and inhibition of NF-κB activity in rats with brain injury.
作者
常毅
田雨
邹佳芮
于洋
周南
张松
CHANG Yi;TIAN Yu;ZU Jia-rui;YU Yang;ZHOU Nan;ZHANG Song(Department of Anesthesiology,Dalian Central Hospital,Dalian 116033;Department of Anesthesiology,General Hospital of the Northern Thealer Command,Shenyang 110016;Rehabilitation Training Division,Dalian Rehabilitation Center,Joint Logistic Support Force,Dalian 116013,China)
出处
《解剖科学进展》
CAS
2022年第2期192-196,共5页
Progress of Anatomical Sciences
基金
辽宁省自然科学基金(20180551091)。
