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Mitochondrial apoptosis pathway involved in apoptosis of human umbilical vein endothelial cell after heat stress / 中华急诊医学杂志
Article in Chinese | WPRIM (Western Pacific) | ID: wpr-470998
Responsible library: WPRO
ABSTRACT
Objective To observe the expressions of cytochrome C,Caspase-9,Caspase-3 and their relationships,and investigate apoptosis signal transduction mechanism after heat stress-induction in human umbilical vein endothelial cell (HUVEC),and explore pathogenesis of vascular endothelial damage in the wake of severe heat stroke.Methods Human umbilical vein endothelial cell heat stress model was set up.Control group were incubated at 37℃,while heat stress group of cells were incubated at 39℃,41℃,and 43℃ for 2h,then all the cells were further incubated at 37℃ for 24 h.Mitochondria of human umbilical vein endothelial cell were examined with electron microscopy.Apoptosis was analyzed by flow cytometry using Annexin V-FITC/PI staining,and protein levels of cytochrome C,caspase-9,caspase-3 were analyzed by western blot.Results In the control group (37℃),the structure of mitochondrial was intact in HUVEC under transmission electron microscope.In contrast,mitochondrial swelling was found in the group of 43℃ heat stress.Compared with control group,as increasing in heat stress temperature,the rates of induced apoptosis were 17.8% at 41℃ and 25.6% at 43℃,and the levels of cytochrome C,Caspase-9,and caspase-3 were significantly increased (P <0.05).There was no obvious change at 39℃ heat stress (P > 0.05).Conclusions Mitochondrial apoptosis pathway is involved in apoptosis of human umbilical vein endothelial cells in the wake of heat stress.The vascular endothelial cells apoptosis may be associated with the occurrence of severe heat stroke.

Full text: Available Database: WPRIM (Western Pacific) Language: Chinese Journal: Chinese Journal of Emergency Medicine Year: 2014 Document type: Article
Full text: Available Database: WPRIM (Western Pacific) Language: Chinese Journal: Chinese Journal of Emergency Medicine Year: 2014 Document type: Article
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