摘要
目的探讨瑞马唑仑对脑缺血再灌注大鼠神经损伤的影响及可能机制。方法将大鼠随机分为假手术组、脑缺血再灌注组、瑞马唑仑组和AMPK抑制剂组,Longa评分评估大鼠神经功能,TTC染色测定脑组织梗死体积比,TUNEL染色检测脑组织细胞凋亡,qRT-PCR法检测脑组织中AMPK/SIRT1/PGC1α通路相关mRNA表达,Western blot方法检测脑组织中AMPK/SIRT1/PGC1α通路相关蛋白表达。结果瑞马唑仑能降低脑缺血再灌注大鼠Longa评分及脑组织梗死体积比、细胞凋亡率,激活脑组织中AMPK/SIRT1/PGC1α通路,AMPK抑制剂削弱了瑞马唑仑对脑缺血再灌注大鼠的影响。结论瑞马唑仑能减轻脑缺血再灌注大鼠的神经损伤,其机制与激活AMPK/SIRT1/PGC1α信号通路有关。
Objective To investigate the influence of remimazolam on nerve injury in rats with cerebral ischemia-reperfusion and its possible mechanism.Methods Rats were randomly divided into sham operation group,cerebral ischemia-reperfusion group,remazolam group and AMPK inhibitor group.The neurological function of rats was assessed by Longa score.Infarct volume ratio of brain tissue was measured by TTC staining,and apoptosis of brain tissue was detected by TUNEL staining.The mRNA expression of AMPK/SIRT1/PGC1αpathway was detected by qRT-PCR,and the protein expression of AMPK/SIRT1/PGC1αpathway was detected by Western blot.Results Remazolam can reduce Longa score,infarct volume ratio and apoptosis rate in cerebral ischemia reperfusion rats,and activate AMPK/SIRT1/PGC1αpathway in brain tissue.AMPK inhibitor can weaken the effect of remazolam on cerebral ischemia reperfusion rats.Conclusion Remimazolam can alleviate the nerve injury in rats with cerebral ischemia-reperfusion,and its mechanism is related to the activation of AMPK/SIRT1/PGC1αsignaling pathway.
作者
时卫刚
李萱
高深
王崇民
郑连红
霍丽民
闫纪琳
SHI Wei-gang;LI Xuan;GAO Shen;WANG Chong-min;ZHENG Lian-hong;HUO Li-min;YAN Ji-lin(Department of Anesthesiology,the First Hospital of Handan,Handan 056002;Department of Neurology,Affiliated Hospital of Hebei University of Engineering,Handan 056008,China)
出处
《解剖科学进展》
CAS
2023年第6期573-576,579,共5页
Progress of Anatomical Sciences
基金
河北省科技厅科技计划项目(17277714D)
邯郸市科技局科学技术研究与发展计划项目(19422083028ZC)。
