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Honokiol protects rat hearts against myocardial ischemia reperfusion injury by reducing oxidative stress and inflammation
Author(s) -
Yun Wang,
Z.Z. Zhang,
Yun Wu,
Jia Zhan,
Xianghu He,
Yanlin Wang
Publication year - 2012
Publication title -
experimental and therapeutic medicine
Language(s) - English
Resource type - Journals
eISSN - 1792-1015
pISSN - 1792-0981
DOI - 10.3892/etm.2012.766
Subject(s) - honokiol , malondialdehyde , myeloperoxidase , oxidative stress , lactate dehydrogenase , reperfusion injury , pharmacology , medicine , superoxide dismutase , ischemia , tumor necrosis factor alpha , creatine kinase , inflammation , chemistry , biochemistry , enzyme
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 κB(NF-κB; 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 (MPO) activity, concentrations of tumor necrosis factor (TNF)-α and interleukin (IL)-6 and expression level of NF-κB 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.

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