[Heat shock pretreatment in inhibiting myocardical apoptosis induced by ischemia-reperfusion and its mechanism].
OBJECTIVE
To explore the mechanisms of myocardial apoptosis during myocardial ischemia-reperfusion injury and to further clarify the molecular mechanisms by which heat shock pretreatment in inhibiting myocardial apoptosis induced by ischemia-reperfusion injury.


METHODS
Myocardial ischemia-reperfusion injury was induced by the occlusion of left anterior descending branch of the coronary artery. Apoptosis was evaluated by DNA laddering assay and the activities of caspase 3, 8, or 9 was measured with Caspase Colorimetric Assay Kit. Expression of heat shock proteins was detected by Western blotting analysis. To explore the effect of heat shock pretreatment on myocardium against apoptosis, mice were pretreated with whole body hyperthermia before the myocardial ischemia-reperfusion injury.


RESULTS
Ischemia-reperfusion injury induced myocardial apoptosis and activation of caspase-3,8,9. Heat shock pretreatment induced the expression of several family members of heat shock proteins and inhibited myocardial apoptosis and activation of the above caspases.


CONCLUSIONS
Mitochondria and death receptor signaling pathways play important roles in myocardial apoptosis induced by ischemia-reperfusion injury. Heat shock pretreatment may increase the expression of several HSP, and inhibit the activation of both mitochondria and death receptor signaling pathways and apoptosis in cardiomyocytes induced by myocardial ischemia-reperfusion injury.
Shi
Yong-zhong
YZ
Department of Pathophysiology, Xiangya School of Medicine, Central South University, Changsha, China.
Xiao
Wei-min
WM
Jiang
Bi-mei
BM
Tang
Dao-lin
DL
Chen
Guang-wen
GW
Xiao
Xian-zhong
XZ
D000818:Animals; D017209:Apoptosis; D053148:Caspase 3 / Q000378:metabolism; D053181:Caspase 8 / Q000378:metabolism; D053453:Caspase 9 / Q000378:metabolism; D006360:Heat-Shock Proteins / Q000096:biosynthesis / Q000378:metabolism; D018869:Heat-Shock Response; D006979:Hyperthermia, Induced; D008297:Male; D051379:Mice; D008929:Mitochondria, Heart / Q000187:drug effects / Q000378:metabolism*; D015428:Myocardial Reperfusion Injury / Q000378:metabolism / Q000473:pathology*; D032383:Myocytes, Cardiac / Q000378:metabolism / Q000473:pathology*; D011897:Random Allocation
D006360:Heat-Shock Proteins; C505409:Casp3 protein, mouse; C505526:Casp8 protein, mouse; C506434:Casp9 protein, mouse; D053148:Caspase 3; D053181:Caspase 8; D053453:Caspase 9