关键词:

川崎病, 红景天苷, 炎症反应, 氧化应激, 肿瘤坏死因子?α, 人冠状动脉内皮细胞

Abstract:

Objective To study the effect of salidroside（Sal）on the inflammatory response and oxidative stress of coronary arteries in Kawasaki disease and its mechanism. Methods The cells were divided into normal control group，TNF⁃ α group，50 μmol/L and 100 μmol/L Sal group. The effect of Sal and TNF⁃ α at different concentrations on HCAEC survival was detected by CCK⁃8. The relative protein expression levels of phosphorylated phosphatidylinositol 3 kinase（p⁃PI3K），phosphorylated protein kinase B（p⁃Akt），phosphorylated NF⁃ κBp65 （p⁃P65），interleukin 6（IL⁃6），IL⁃1β，tight junction protein（ZO⁃1）and vascular endothelial calherin（VE⁃cad⁃ herin）were detected by Western blot. The expression levels of inflammatory factors and adhesion molecule mRNAs were detected by RT⁃qPCR. Intracellular reactive oxygen species（ROS）production was observed by DCFH⁃DA fluorescent probes. Intracellular superoxide dismutase（SOD）and glutathione peroxidase（GSH⁃Px）were analyzed with spectrophotometers. Results Compared with the control group ，the protein expression levels of p⁃PI3K， p⁃Akt，ZO⁃1 and VE⁃cadherin were significantly reduced（P < 0.05），the protein expression levels of p⁃P65，IL⁃6 and IL⁃1β were significantly increased（P < 0.05），and the mRNA expression levels of IL⁃6，IL⁃8，IL⁃1β，ICAM⁃ 1，and VCAM ⁃1 were significantly increased（P < 0.05）. The generation of ROS was significantly increased and the viability of SOD and GSH⁃Px were significantly decreased in the TNF⁃α group（P < 0.05），while Sal could significantly reverse these effects. Conclusion Salidroside can attenuate TNF⁃α⁃induced inflammatory response and oxidative stress levels in HCAEC cells probably by way of activating PI3K/Akt and inhibiting NF⁃ κB signal⁃ ing pathway.

Key words:

Kawasaki disease, salidroside, inflammatory response, oxidative stress, tumor necro? sis factor?α, human coronary artery endothelial cells