The attenuation of myocardial susceptibility to ischemia/reperfusion injury by ischemic postconditioning in hypercholesteremia rats and the role of hypoxia inducible factor-1alpha.
- Author:
Huan-Xin ZHAO
1
,
2
;
Xiao-Yu LI
;
Ye WU
;
Xiao-Liang WANG
;
Rong-Rui ZHAO
;
Hui-Rong LIU
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Apoptosis; Caspase 3; metabolism; Creatine Kinase; metabolism; Disease Susceptibility; Hypercholesterolemia; metabolism; Hypoxia-Inducible Factor 1, alpha Subunit; metabolism; Ischemic Postconditioning; Male; Myocardial Reperfusion Injury; prevention & control; Rats; Rats, Wistar
- From: Chinese Journal of Applied Physiology 2012;28(4):319-327
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo explore whether ischemic postconditioning can attenuate the myocardial injury induced by ischemia/reperfusion (I/R) in hypercholesteremic rats and whether hypoxia inducible factor-1alpha (HIF-1alpha) play a role in the protection.
METHODSAdult male Wistar rats received a high fat diet for 8 weeks to prepare the hypercholesteremic models. Myocardial damage induced by ischemia/reperfusion was evaluated by infarct size, creatine kinase (CK) activity and myocardial apoptosis. HIF-1alpha mRNA level was detected by real time-RT-PCR and the protein level was detected by Western blot.
RESULTSMyocardial infarct size, CK activity, and caspase-3 activity induced by I/R were markedly increased in hypercholesteremic rats compared with those in normal rats. Ischemic postconditioning attenuated the myocardial injury in both normal rats and hypercholesteremic rats, and increased HIF-1alpha protein level. There was a significant linear inverse relationship between HIF-1alpha protein level and infarct size (r = -0.802, P <0.01).
CONCLUSIONHypercholesteremia enhanced the susceptibility of myocardia to ischemia/reperfusion injury. While ischemic postconditioning markedly attenuated the increase of myocardial susceptibility to I/R induced by hypercholesteremia. HIF-1alpha might be one of the mechanisms of protection by ischemic postconditioning.
