Necroptosis mediates high glucose-induced injury in human umbilical vein endothelial cells
10.3969/j.issn.1000-4718.2016.09.013
- VernacularTitle:坏死性凋亡介导高糖引起的人脐静脉内皮细胞损伤
- Author:
Jiaqiong LIN
;
Meiji CHEN
;
Ruixian GUO
;
Weijie ZHANG
;
Ximei ZHI
;
Haiou DENG
;
Ling XU
;
Yinglan LI
;
Wen WU
- Publication Type:Journal Article
- Keywords:
Necroptosis;
Apoptosis;
High glucose;
HUVECs;
Necrostatin-1
- From:
Chinese Journal of Pathophysiology
2016;32(9):1608-1613
- CountryChina
- Language:Chinese
-
Abstract:
AIM: To explore whether necroptosis contributes to the high glucose (HG)-induced damage in hu-man umbilical vein endothelial cells (HUVECs).METHODS: The protein levels of receptor-interacting protein 3 (RIP3) and cleaved caspase-3 were detected by Western blot.The intracellular levels of reactive oxygen species (ROS) were deter-mined by DCFH-DA staining followed by photofluorography.Mitochondrial membrane potential (MMP) was measured by rhodamine 123 staining followed by photofluorography.RESULTS: Treatment of HUVECs with HG at different concentra-tions (10, 20 and 40 mmol/L glucose) for 24 h gradually enhanced the expression levels of RIP3.Treatment of HUVECs with HG (40 mmol/L glucose) for different time (3 h, 6 h, 9 h, 12 h and 24 h) also up-regulated the expression levels of RIP3, peaking at 9 h.Pretreatment of HUVECs with 20 μmol/L Z-VAD-FMK (an inhibitor of caspase) for 30 min before exposure to HG enhanced the expression level of RIP3.Pretreatment of HUVECs with 100 μmol/L necrostatin-1 (an inhi-bitor of necroptosis) for 1 h before exposure to HG alleviated the HG-induced injuries, such as a decrease in cell viability, an increase in ROS generation and dissipation of MMP, but up-regulated the protein level of cleaved caspase-3.CON-
CLUSION: Necroptosis mediates HG-induced injury in HUVECs.There is a negative interacting between necroptosis and apoptosis.