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Abstract

Acanthopanax senticosus Protects Against Myocardial Ischemia Reperfusion Injury in Rats

Author(s): HONGYING WU1 AND MIN ZHANG
Geriatrics Department, Outpatient Department, Sichuan Academy of Medical Sciences, Sichuan People's Hospital, West Second Section of The First Ring Road 32, Chengdu, 610072, China

Correspondence Address:
Outpatient Department, Sichuan Academy of Medical Sciences, Sichuan People's Hospital, West Second Section of The First Ring Road 32, Chengdu, 610072, China, E-mail: [email protected]

The protective effects of Acanthopanax senticosus on myocardial ischemia reperfusion injury in rats was explored. A total of 60 male Sprague Dawley rats were randomly divided into the sham operated group (group C), the ischemia reperfusion group (group IR), the Acanthopanax senticosus plus blocker group (group ASS+Z), and the Acanthopanax senticosus group (group ASS). The rat myocardial ischemia reperfusion injury models were established through ligating left anterior descending branches of coronary artery in rats. TUNEL assay and Western Blot was used to detect the apoptotic index of myocardial cells and the expression levels of extracellular regulating kinase 1/2 (ERK1/2) and phosphorylation ERK1/2 (p-ERK1/2). Meanwhile, a total of 30 rats were randomly selected and divided into 5 groups; the control group (group c) was the simple ischemia reperfusion group, while groups P1, P2, P3, and P4 were given different dosage concentrations of Acanthopanax senticosus for pre-adaptation. The Langendorff isolated heart perfusion model was used to record the dynamic changes in cardiac functions and coronary artery flow in each group. The results have shown that the Acanthopanax senticosus had certain protective effects on the ischemia reperfusion injury of rat myocardium, as well as the pre-adaptive effects on the systolic functions of left ventricles after reperfusion, which would increase coronary flow and resist the arrhythmia, thereby reducing the apoptosis rates of myocardial cells and protecting the myocardium through activating the ERK1/2 pathway.

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