Abstract
Achyranthes bidentata, a Chinese medicinal herb, is reported to be neuroprotective. However, its role in cardioprotection remains largely unknown. Our present study aimed to investigate the effects of Achyranthes bidentata polypeptides (ABPP) preconditioning on myocardial ischemia/reperfusion (MI/R) injury and to test the possible mechanisms. Rats were treated with ABPP (10 mg/kg/d, i.p.) or saline once daily for one week. Afterward, all the animals were subjected to 30 min of myocardial ischemia followed by 4 h of reperfusion. ABPP preconditioning for one week significantly improved cardiac function following MI/R. Meanwhile, ABPP reduced infarct size, plasma creatine kinase (CK)/lactate dehydrogenase (LDH) activities and myocardial apoptosis at the end of reperfusion in rat hearts. Moreover, ABPP preconditioning significantly inhibited superoxide generation, gp91phox expression, malonaldialdehyde formation and enhanced superoxide dismutase activity in I/R hearts. Furthermore, ABPP treatment inhibited PTEN expression and increased Akt phosphorylation in I/R rat heart. PI3K inhibitor wortmannin blocked Akt activation, and abolished ABPP-stimulated anti-oxidant effect and cardioprotection. Our study demonstrated for the first time that ABPP reduces oxidative stress and exerts cardioprotection against MI/R injury in rats. Inhibition of PTEN and activation of Akt may contribute to the anti-oxidant capacity and cardioprotection of ABPP.
Highlights
Myocardial infarction (MI) remains one of the leading causes of death and disability throughout the world
Antioxidant enzyme superoxide dismutase (SOD) activity in cardiac tissue was increased in I/R rats with Achyranthes bidentata polypeptides (ABPP) preconditioning (Figure 4D). These results demonstrated that ABPP reduced superoxide overproduction and decreased oxidative stress in I/R hearts
These results indicated that ABPP preconditioning inhibited PTEN expression and activated survival Akt signaling following myocardial ischemia/reperfusion (MI/R)
Summary
Myocardial infarction (MI) remains one of the leading causes of death and disability throughout the world. The process of restoring blood flow to the ischemic myocardium, can induce injury, myocardial reperfusion injury, which can paradoxically reduce the beneficial effects of myocardial reperfusion and cause contractile dysfunction and cellular damage [1,2,3]. Evidence has shown that MI/R promotes excess generation of highly ROS and causes oxidative stress which further exacerbates the development and progression of cardiopathy and its complications [6]. The effects of ABPP on oxidative stress following MI/R remain unknown. It is widely accepted that activation of the phosphatidylinositol-3-kinase (PI3K)/protein kinase B (Akt) pathway regulates myocardial oxidative stress and contributes to the cardioprotection against. Whether ABPP regulates PTEN and Akt signaling following MI/R in vivo remains unknown. The present study was designed to investigate whether ABPP exerts cardioprotection against MI/R injury and the underlying mechanisms
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