右美托咪定调控miR-132-3p对缺氧复氧诱导的脑微血管细胞损伤的影响

Effects of Dexmedetomidine-Regulated MiR-132-3p on Cerebral Microvascular Cell Injury Induced by Hypoxia and Reoxygenation

目的:右美托咪定(Dex)调控miR-132-3p对缺氧复氧(H/R)诱导的脑微血管细胞(HBMEC)损伤的影响。方法:体外培养人HBMEC,用低、中、高剂量(0.01、0.10、1.00μmoL/L)Dex干预后,建立H/R损伤模型;转染miR-NC、miR-132-3p至HBMEC,建立H/R模型;转染anti-miR-NC、anti-miR-132-3p,用1.00μmoL/L Dex干预后,建立H/R损伤模型。ELISA检测IL-1β、IL-6、TNF-α水平;试剂盒检测MDA、SOD、CAT水平;RT-qPCR检测细胞miR-132-3p表达。结果:HBMEC经H/R诱导后,IL-1β、IL-6、TNF-α、MDA水平升高(P<0.05),SOD、CAT水平降低(P<0.05),miR-132-3p表达水平降低(P<0.05);Dex干预后,H/R诱导的HBMEC中IL-1β、IL-6、TNF-α、MDA水平降低(P<0.05),SOD、CAT水平升高(P<0.05),miR-132-3p表达水平升高(P<0.05)。上调miR-132-3p后,H/R诱导的HBMEC中IL-1β、IL-6、TNF-α、MDA水平降低(P<0.05),SOD、CAT水平升高(P<0.05)。下调miR-132-3p逆转Dex对H/R诱导的HBMEC炎症因子表达及氧化应激的影响。结论:Dex上调miR-132-3p抑制H/R诱导的人脑微血管内皮细胞损伤。

Objective:To study the effect of dexmedetomidine(Dex)regulateing miR-132-3p on the damage of cerebral microvascular cells(HBMEC)induced by hypoxia and reoxygenation(H/R).Methods:Human HBMEC were cultured in vitro and intervened with low,medium and high doses(0.01,0.10,1.00μmol/L)of Dex to establish H/R injury models.The miR-NC or miR-132-3p mimics were transfected into HBMEC to establish H/R injury models.After HBMEC were transfected with anti-miR-NC or anti-miR-132-3p,they were intervened with 1.00μmol/L Dex,and then H/R injury models was established.The levels of IL-1β,IL-6 and TNF-αwere detected by ELISA;the levels of MDA,SOD and CAT were detected by the kit;the expression of miR-132-3p was detected by RT-qPCR.Results:After HBMEC was induced by H/R,the levels of IL-1β,IL-6,TNF-αand MDA were increased(P<0.05),but the levels of SOD and CAT were decreased(P<0.05),and the expression level of miR-132-3p was decreased(P<0.05).After Dex intervention,the levels of IL-1β,IL-6 TNF-αand MDA in H/R-induced HBMEC decreased(P<0.05),but the levels of SOD and CAT increased(P<0.05),and the expression level of miR-132-3p increased(P<0.05).After up-regulation of miR-132-3p,the levels of IL-1β,IL-6 TNF-αand MDA in H/R-induced HBMEC decreased(P<0.05),but the levels of SOD and CAT increased(P<0.05).Down-regulation of miR-132-3p reversed the effects of Dex on H/R-induced inflammatory factor expression and oxidative stress in HBMECs.Conclusion:Dex could inhibit H/R-induced injury of human brain microvascular endothelial cells by up-regulating miR-132-3p.