Gossypol alleviates isolated heart ischemia/reperfusion injury in rats by interfering with the oxidative stress response and suppressing the JNK/p38 MAPK signal pathway
10.19405/j.cnki.issn1000-1492.2017.10.002
- VernacularTitle:棉子酚通过干扰氧化应激反应、抑制JNK/p38MAPK信号通路的激活减轻大鼠离体心脏缺血再灌注损伤
- Author:
Leilei JIA
1
;
Ailing WANG
Author Information
1. 安徽医科大学第一附属医院心内科
- Keywords:
Gossypol;
myocardial ischemia/reperfusion injury;
oxidative stress response;
JNK/p38 MAPK signal pathway
- From:
Acta Universitatis Medicinalis Anhui
2017;52(10):1424-1429
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the protective effect and possible mechanism of Gossypol on isolated myocardial ischemia/reperfusion injury in rats.Methods 40 male Sprague-Dawley rats were randomly divided into 4 groups:Blank group,heart ischemia reperfusion group (MI/R group),high and low-dose Gossypol group (40,20 mg/L).The model of the myocardial ischemia/reperfusion injury were established using the Langendorff method.The hemodynamicsindexes,cardiac enzymes AST and LDH,inflammatory cytokines (NF-κB,ICAM-1,TNF-α and IL-6) were measured.The effect and mechanism of Gossypol on early-stage MI/R of the oxidative stress response and the JNK/p38 MAPK signal pathway were investigated.Results Experimental results showed that Gossypol could significantly improve the functional capacity of the heart,reduce the contents of AST,LDH and inflammatory cytokines in reperfused heart tissue,and increase superoxide dismutase levels to protect the heart.The mechanism of this substance may involve anti-lipid peroxidation and inhibition of p38 kinase phosphorylation and JNK,and reduction of oxidative stress injury and apoptosis damage induced by MI/R.Conclusion This study confirm that Gossypol exerts extensive anti-MI/R effects.Its mechanism may be related to the interfering with the oxidative stress response and suppressing the JNK/p38 MAPK signal pathway.
