摘要
目的 研究咪达唑仑轮对于脂多糖(lipopolysaccharide,LPS)诱导的H9c2心肌细胞损伤的作用及其分子生物学机制.方法 比较经不同浓度、不同时间的咪达唑仑和LPS刺激的H9c2细胞活力以确定达唑仑最佳给药条件;将H9c2心肌细胞分为对照组、咪达唑仑组、LPS组和LPS+咪达唑仑组,比较各组细胞凋亡率、线粒体膜电位变化情况、氧化应激指标、炎性因子水平和NOD样受体蛋白3(NOD-like re-ceptor protein3,NLRP3)/胱天蛋白酶1(caspase-1)途径相关蛋白表达水平,并用NLRP3激活剂尼日利亚菌素验证咪达唑仑的作用.结果 咪达唑仑可降低LPS介导的H9c2心肌细胞凋亡率,减轻氧化应激和炎性反应,提高NLRP3/caspase-1通路相关蛋白表达水平.结论 咪达唑仑对LPS介导的H9c2心肌细胞损伤具有保护作用,其作用机制可能与抑制NLRP3/caspase-1通路相关.
Objective To study the effect of midazolam on lipopolysaccharide(LPS)-induced H9c2 cardiomyocyte damage and its molecular biological mechanism.Methods H9c2 cell viability was compared under stimulation with midazolam and LPS at different concentrations and time points to determine the optimal administration conditions for midazolam.H9c2 cardiomyocytes were divided into control group,midazolam group,LPS group and LPS+midazolam group.Cell apoptosis rate,mitochondrial membrane potential changes,oxidative stress indicators,levels of inflammatory factors and expression levels of NOD-like receptor protein3(NLRP3)/caspase-1 pathway-related proteins were compared among the groups.The effect of midazolam was validated with NLRP3 activator nigericin.Results Midazolam can reduce the apoptosis rate of LPS-induced H9c2 cardiomyocytes,alleviate the oxidative stress response and inflammatory response,and enhance the expression levels of NLRP3/caspase-l pathway-related proteins.Conclusion Midazolam has a protective effect on LPS-induced H9c2 cardiomyocyte damage.Its mechanism may be related to the inhibition of NLRP3/caspase-1 signaling pathway.
作者
王希
闫战秋
贾旺
全燕
WANG Xi;YAN Zhanqiu;JIA Wang;QUAN Yan(Department of Anesthesiology,Qinhuangdao Maternal and Child Health Care Hospital,Qinhuangdao,Hebei,066000,China)
出处
《医学分子生物学杂志》
CAS
2022年第4期269-275,共7页
Journal of Medical Molecular Biology
基金
秦皇岛市卫生健康委员会项目(No.202003B035)。
