摘要
目的探讨异氟烷(isoflurane,ISO)对缺氧/复氧(hypoxia/reoxygenation,H/R)损伤人肝细胞的作用及相关机制。方法将人肝细胞系HL-7702分为对照组(Con)、H/R组和不同浓度(0.5%、1%和1.5%)ISO组。用MTT法检测细胞活力,LDH试剂盒法检测LDH活性,ROS探针法检测ROS生成水平,TUNEL染色法检测细胞凋亡,Western blot法检测TLR4、FADD、MyD88和TRAf6表达水平。结果与Con组比较,H/R组细胞活力降低,LDH活性、ROS水平、凋亡细胞比例以及TLR4、FADD、MyD88和TRAf6表达水平均增加;ISO可以缓解H/R导致的肝细胞活力降低、LDH活性、ROS水平和凋亡细胞升高以及TLR4、FADD、MyD88和TRAf6表达水平增加。结论ISO可通过降低氧化应激和下调TLR4、FADD、MyD88和TRAf6表达水平来减轻肝细胞H/R损伤。
Objective To explore the effect and the mechanism of isoflurane(ISO)on human liver cells(HL-7702)injury induced by hypoxia/reoxygenation(H/R).Methods HL-7702 cells were divided into control group(Con),hypoxia/reoxygenation(H/R)and various concentrations(0.5%,1%,1.5%)ISO treatment group.Cell viability,LDH activity,ROS production,apoptosis and the expression levels of TLR4,FADD,MyD88 and TRAf6 were detected using MTT assay,LDH activity assay kit,ROS Probe,TUNEL staining and Western blot,respectively.Results Compared with Con group,the cell viability was decreased,LDH activity,ROS production level,proportion of apoptotic cells,and the expression levels of TLR4,FADD,MyD88 and TRAf6 were increased in H/R group.ISO relieved the decrease of cell viability,the increase of LDH activity,ROS production and apoptosis cells,and the down-regulation the protein expression levels of the TLR4,FADD,MyD88 and TRAF6 induced by H/R.Conclusion ISO can reduce H/R injury in the hepatocytes by reducing oxidative stress and down-regulating the expression levels of TLR4,FADD,MyD88 and TRAF6.
作者
王彦利
师爱青
张咸虎
Wang Yanli;Shi Aiqing;Zhang Xianhu(Department of Anesthesiology,Central Hospital of Jiaozuo Coal Industry Group Co.,Ltd,Jiaozuo 454000)
出处
《中国组织化学与细胞化学杂志》
CAS
CSCD
2021年第5期449-454,共6页
Chinese Journal of Histochemistry and Cytochemistry
