Exogenous hydrogen sulfide attenuates high glucose-induced injury by in-hibiting JAK/STAT pathway in human umbilical vein endothelial cells
10.3969/j.issn.1000-4718.2016.07.002
- VernacularTitle:外源性硫化氢通过抑制JAK／STAT通路对抗高糖引起的人脐静脉内皮细胞损伤
- Author:
Jiaqiong LIN
;
Jingfu CHEN
;
Jingqiu LIAO
;
Kai LIN
;
Haiou DENG
;
Dongbo WU
;
Wen WU
- Publication Type:Journal Article
- Keywords:
Hydrogen sulfide;
JAK/STAT pathway;
High glucose;
Human umbilical vein endothelial cells
- From:
Chinese Journal of Pathophysiology
2016;32(7):1161-1166
- CountryChina
- Language:Chinese
-
Abstract:
AIM: To explore whether exogenous hydrogen sulfide (H2S) depresses high glucose (HG)-in-duced injury by modulating the Janus kinase/signal transducer and activator of transcription ( JAK/STAT) pathway in hu-man umbilical vein endothelial cells (HUVECs).METHODS:The protein levels of JAK2, STAT3 and cleaved caspase-3 were determined by Western blot.The cell viability was measured by CCK-8 assay.Mitochondrial membrane potential ( MMP) was detected by rhodamine 123 staining followed by photofluorography.The intracellular level of reactive oxygen species (ROS) was analyzed by DCFH-DA staining followed by photofluorography.The activity of superoxide dismutase (SOD) was also measured.RESULTS:Pretreatment of the HUVECs with 400 μmol/L NaHS (a donor of H2S) for 30 min prior to exposure to 40 mmol/L glucose ( HG) markedly attenuated HG-induced upregulation of the phosphorylation of JAK2 and STAT3.Pretreatment with 400μmol/L NaHS for 30 min or with 20μmol/L AG490 (inhibitor of the JAK/STAT pathway) for 30 min attenuated the injury of HUVECs induced by HG, as indicated by the increases in cell viability and SOD activity, and decreases in the protein level of cleaved caspase-3, ROS generation and dissipation of MMP.CONCLU-SION:Exogenous H2 S protects HUVECs against HG-induced injury by inhibiting JAK/STAT pathway.
