Honokiol protects rat hearts against myocardial ischemia reperfusion injury by reducing oxidative stress and inflammation

被引:70
作者
Wang, Yun [1 ]
Zhang, Zhong-Ze [1 ]
Wu, Yun [1 ]
Zhan, Jia [1 ]
He, Xiang-Hu [1 ]
Wang, Yan-Lin [1 ]
机构
[1] Wuhan Univ, Dept Anesthesiol, Zhongnan Hosp, Wuhan 430071, Hubei, Peoples R China
基金
中国国家自然科学基金;
关键词
honokiol; ischemia/reperfusion; oxidative inflammation; NF-kappa B; NF-KAPPA-B; ISCHEMIA/REPERFUSION INJURY; CEREBRAL-ISCHEMIA; ACTIVATION; MAGNOLOL; OXYGEN; INHIBITION; EXPRESSION; SURVIVAL; NECROSIS;
D O I
10.3892/etm.2012.766
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Honokiol, a potent radical scavenger, has been demonstrated to ameliorate cerebral infarction following ischemia/reperfusion (I/R) injury. However, its effects on myocardial I/R injury remain unclear. The present study aimed to examine the effects of honokiol on myocardial I/R injury and to investigate its potential cardioprotective mechanisms. Sprague-Dawley rats were pretreated with honokiol and exposed to a 30-min myocardial ischemia followed by 2-h coronary reperfusion. Myocardial I/R-induced infarct size and biochemical and histological changes were compared. The expression of nuclear factor kappa B(NF-kappa B; p65) was assessed by western blotting. Pretreatment with honokiol significantly reduced infarct size, and serum creatine kinase (CK) and lactate dehydrogenase (LDH) release compared with those in the I/R group following a 2-h reperfusion. The malondialdehyde (MDA) level, myeloperoxidase (M PO) activity, concentrations of tumor necrosis factor (TNF)-alpha and interleukin (IL)-6 and expression level of NF-kappa B were all reduced by honokiol pretreatment, while honokiol inhibited the decreases in superoxide dismutase (SOD) and catalase (CAT) activities. In addition, less neutrophil infiltration and histopathological damage in the myocardium were observed in the honokiol-pretreated group. These findings indicate that honokiol pretreatment diminished myocardial I/R injury through attenuation of oxidative stress and inflammation.
引用
收藏
页码:315 / 319
页数:5
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