Abstract: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, 1.00 μmol/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 1.00 μmol/L Dex, and then H/R injury models was established. The levels of IL-1β, IL-6 and TNF-α were 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-α and 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-α and 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-α and 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.
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