Effect of curcumin on ox-LDL-induced HAEC injury
10.3969/j.issn.1000-4718.2017.08.003
- VernacularTitle:姜黄素减轻氧化型低密度脂蛋白诱导的人主动脉内皮细胞损伤
- Author:
Yong HU
;
Xiaohong SU
;
Huolan ZHU
;
Lingxiao ZHANG
;
Fei LIU
;
Zhongwei LIU
- Keywords:
Curcumin;
Human aortic endothelial cells;
Oxidized low-density lipoprotein;
Peroxisome prolife-rator-activated receptor γ
- From:
Chinese Journal of Pathophysiology
2017;33(8):1359-1364
- CountryChina
- Language:Chinese
-
Abstract:
AIM: To investigate the effect of curcumin on oxidized low-density lipoprotein (ox-LDL)-induced injury of human aortic endothelial cells (HAECs).METHODS: HAECs were pre-treated with curcumin at different concentrations and then treated with ox-LDL.The cell viability was assessed by MTT assay.The cell proliferation ability was analyzed by EdU assay.ELISA was used to determine the concentrations of interleukin-6 (IL-6), transforming growth factor β1 (TGFβ1), high mobility group box-1 protein (HMGB1) and secretory receptor for advanced glycation end products (sRAGE) in the HAEC culture medium.The binding activity of peroxisome proliferator-activated receptor γ (PPARγ) was evaluated by electrophoretic mobility shift assay.The protein levels of HO-1, HMGB1, RAGE,IL-6,TGFβ1 and phosphorylated PPARγ in the HAECs were determined by Western blot.RESULTS: The viability and the proliferation ability decreased significantly in the HAECs treated with ox-LDL.The PPARγ/HO-1 signaling pathway was inhibited while its down-stream HMGB1/RAGE signaling pathway was activated by ox-LDL.The levels of IL-6, TGFβ1, HMGB1 and sRAGE were increased.Pre-treatment with curcumin activated PPARγ/HO-1 signaling pathway and inhibited HMGB1/RAGE signaling pathway in ox-LDL treated HAECs in a concentration-dependent manner.The levels of IL-6, TGFβ1, HMGB1 and sRAGE were also decreased dramatically by pre-treatment of curcumin in a concentration-dependent manner.CONCLUSION: ox-LDL induces HAEC damage by inhibiting PPARγ/HO-1 to activate HMGB1/RAGE inflammatory signaling.Curcumin exerts protective effect on ox-LDL treated HAECs via activating PPARγ/HO-1 signaling pathway.
