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Annals of Vascular Surgery 2016-Jul

Cardioprotective Effects of Phenylethanoid Glycoside-rich Extract from Cistanche deserticola in Ischemia-Reperfusion-Induced Myocardial Infarction in Rats.

Només els usuaris registrats poden traduir articles
Inicieu sessió / registreu-vos
L'enllaç es desa al porta-retalls
Qian Yu
Xin Li
Xia Cao

Paraules clau

Resum

BACKGROUND

The aim of the study was to examine and confirm the cardioprotective effect and mechanism of phenylethanoid glycoside-rich extract of Cistanche deserticola (PhG-RE), a well-known natural antioxidant-based active constituents, against ischemia/reperfusion injury using both in vivo and in vitro approaches.

METHODS

A total of 30 Sprague-Dawley rats were divided in to 3 groups as group 1: sham laparotomy, group 2: IR, and group 3: IR + PhG-RE group (0.25 mg/mL/min). Hearts were subjected to 30 min of global ischemia followed by 45 min of reperfusion. The myocardial infarct size and the activities of creatine kinase isoenzyme (CK-MB) and lactate dehydrogenase (LDH) were measured. Myocardial tissue malondialdehyde (MDA), glutathione peroxidase (GSH-Px), and superoxide dismutase (SOD) levels were detected. Western blot analysis was carried out to determine the cardioprotective mechanisms of PhG-RE.

RESULTS

Hearts treated with PhG-RE showed a significant reduction in infarct size and decrease in CK-MB and LDH activities. PhG-RE also reduced MDA levels and elevated the activities of GSH-Px, SOD. The expressions of cytochrome-c were significantly reduced in the treated group. A significant upregulation of antiapoptotic proteins Bcl-2/Bax with simultaneous downregulation of cleaved-caspase-3 was observed. The molecular signaling cascade, including phospho-Akt (ser-473) and phospho-GSK3β that lead to the activation or suppression of apoptotic pathway, also showed a significant protective role in the treatment group.

CONCLUSIONS

The results suggested that the PhG-RE may reduce the oxidative stress in the reperfused myocardium and play a significant role in the inhibition of apoptotic pathways leading to cardioprotection.

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