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Objective To investigate whether propofol inhibits the expression of miR-141-3p and reduces the molecular mechanism of hypoxia-induced inflammation and apoptosis of pheochromocytoma cell line PC12. Methods PC12 cells were divided into control group, hypoxia group, (5, 10, 20)μmol/L propofol+hypoxia group, anti-miR-con+hypoxia group, anti-miR-141-3p+hypoxia group, miR-con+20 μmol/L propofol+hypoxia group, miR-141-3p+20 μmol/L propofol+hypoxia group. Flow cytometry was used to detect the apoptosis of PC12 cells; Western blot was employed to determine the expression of activated cleaved caspase-3 (cleaved caspase-3) protein, and the kits were implemented to monitor malondialdehyde (MDA) content and superoxide dismutase (SOD) activity; Reactive oxygen species fluorescent probe DCFH-DA method to determine reactive oxygen species (ROS) content; ELISA kits to assay tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, IL-6 content, RT-qPCR to detect the expression of miR-141-3p. Results Compared with the control group, the apoptosis rate, cleaved caspase-3 protein expression level, MDA, ROS, TNF-α, IL-1β, IL-6 content and miR-141-3p expression of PC12 cells in hypoxia group were all increased, while SOD activity weakened (PPPPConclusions Propofol can alleviate the inflammatory response, oxidative stress and apoptosis of PC12 cells induced by hypoxia by inhibiting the expression of miR-141-3p.