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目的探讨白藜芦醇(RSV)对低氧内皮细胞炎症反应的影响及机制。方法 HUVECs分为常氧、低氧、低氧+DMSO、低氧+RSV(低、中、高剂量)组。分别采用CCK8法检测细胞活力,qRT-PCR及Western blot法检测SIRT1、IL-6和ICAM-1 mRNA及SIRT1、PGC-1α和NF-κB p65蛋白的表达,流式细胞术检测活性氧(ROS)含量。结果低氧能抑制HUVECs细胞活力,下调SIRT1、PGC-1α蛋白表达(P<0.05);上调IL-6、ICAM-1 mRNA及磷酸化NF-κB p65蛋白表达(P<0.05);促进ROS生成(P<0.05)。RSV能促进低氧HUVECs细胞活力,上调SIRT1、PGC-1α表达(P<0.05);下调IL-6、ICAM-1及磷酸化NF-κB p65蛋白的表达(P<0.05);抑制ROS生成(P<0.05)。结论 RSV可促进低氧HUVECs细胞活力,其机制可能与RSV抑制低氧HUVECs炎症反应有关。
Objective To investigate the effect and mechanism of resveratrol (RSV) on inflammatory reaction in hypoxia endothelial cells. Methods HUVECs were divided into normoxia, hypoxia, hypoxia + DMSO, hypoxia + RSV (low, medium and high dose) groups. The cell viability was detected by CCK8 assay. The expressions of SIRT1, IL-6 and ICAM-1 mRNA and SIRT1, PGC-1α and NF-κB p65 protein were detected by qRT-PCR and Western blot respectively. )content. Results Hypoxia inhibited the viability of HUVECs and down-regulated the expression of SIRT1 and PGC-1α (P <0.05), upregulated the expression of IL-6 and ICAM-1 mRNA and phosphorylated NF-κB p65 (P <0.05). RSV could promote the cell viability, up-regulate the expression of SIRT1 and PGC-1α (P <0.05), down-regulate the expression of IL-6, ICAM-1 and phosphorylation of NF-κB p65 in HUVECs (P < P <0.05). Conclusions RSV can promote the cell viability in hypoxic HUVECs. The mechanism may be related to the inhibition of RSV on the inflammatory response in HUVECs.