The effect and mechanisms of 20-HETE on myocardial ischemia reperfusion injury
10.3969/j.issn.1671-8348.2015.32.001
- VernacularTitle:20-HETE在心肌缺血再灌注损伤中的作用及机制研究
- Author:
Yong HAN
;
Lirong GUO
;
Deying KONG
;
Hui JIANG
;
Hong TIAN
- Publication Type:Journal Article
- Keywords:
arachidonic acids;
reperfusion injury;
reactive oxygen species;
protein carbonylation
- From:
Chongqing Medicine
2015;(32):4465-4468
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect of 20‐HETE on the isolated myocardial ischemia reperfusion injury and to ex‐plore its underlying mechanisms .Methods Experiments were performed in isolated rat hearts subjected to 35 min of ischemia fol‐lowed by 40 min of reperfusion in Langendorff preparations .HET0016 (1 μmol/L) and various concentrations (10 ,30 or 50 nmol/L) of 20‐HETE were infused 10 min before the onset of ischemia and throughout the reperfusion period .Cardiac hemodynamic changes and myocardial contractility were continuously recorded with the Powerlab /8P system .Myocardial infarct size was meas‐ured by TTC staining .The level of ROS and the protein carbonyl content were determined by DHE fuorescence and DNPH method , respectively .Results Perfusion with HET0016 significantly improved myocardial ischemia reperfusion injury reduction in cardiac contractility ,after inhibited the production of 20‐HETE significantly reduced the occurrence of myocardial infarction area (P<0 .05) ,but exogenous join 20‐HETE aggravated I/R‐induced myocardial injury (P<0 .05) .Myocardial ischemia reperfusion injury significantly increased production of ROS and oxidative stress ,both of which were significantly inhibited by HET 0016 and enhanced by 20‐HETE administration(P< 0 .05) .Conclusion 20‐HETE stimulates ROS production and enhance protein carbonylation , which aggravates myocardial ischemia reperfusion injury .
