Affiliations: [a] Department of Medical Care Center, Hainan Provincial People’s Hospital, Haikou, China
| [b] Department of Pediatrics, Hainan Maternal and Child Health Hospital, Haikou, China
Correspondence:
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Corresponding author: Min Zeng, Department of Medical Care Center, Hainan Provincial People’s Hospital. No.19, Xiuhua Road, Xiuying District, Haikou 570311, China. Tel.:+86 0898 68622312; Fax:+86 0898 6862372; mzdr_sea06@163.com.
Note: [1] These authors contributed equally to this study.
Abstract: This study aimed to investigate the effects of arachidonic acid metabolite epoxyeicosatrienoic acid (EETs) in the apoptosis of endothelial cells induced by tumor necrosis factor-alpha (TNF-α). After human umbilical vein endothelial cells were cultured, TNF-α/ActD, 14, 15-EET, and HMR-1098 were added, respectively, into the culture medium. The apoptosis level of endothelial cells was detected by flow cytometry. After TNF-α/ActD induced endothelial cell apoptosis, flow cytometry staining showed that endothelial cell apoptosis increased significantly, and the apoptotic cells were significantly reduced after the addition of 14, 15-EET. However, the apoptotic cells significantly increased after the addition of HMR-1098. Western Blot results showed that the phosphorylation levels of LC3-II and AMPK were increased after TNF-α/ActD induction, and the increase was noticeable after the addition of 14, 15-EET. However, the phosphorylation levels of LC3-II and AMPK significantly decreased after the addition of HMR-1098. The activity of Caspase-8 and -9 decreased significantly after the addition of 14, 15-EET but increased after the addition of HMR-1098. Arachidonic acid can inhibit TNF-α induced endothelial cell apoptosis by upregulating autophagy.
