Cramming the causative mechanism of glycogen synthase kinase-3β mediated by ischemic preconditioning against ovariectomy challenged rat heart
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Glycogen synthase kinase-3β, Estrogens, Ischemic preconditioning, Mitochondria
Abstract
High risks of cardiovascular diseases in women are associated with low estrogen levels. Ischemic preconditioning (IPC) exhibits protection in the heart by Glycogen synthase kinase-3β (GSK-3β) phosphorylation that inhibits the mPTP opening, and this protective action of IPC is attenuated by estrogen deficiency. An experiment was performed on female Wistar rats with/without ovariectomy (OVX). Isolated rat heart was attached with perfusion assembly. Infract size, coronary flow, LDH, CKMB and histopathology were estimated. Sham control group decreased the LDH, CKMB and infract size in normal rat heart. The IPC mediated protection of heart was attenuated in OVX rat heart. Inhibition of GSK-3β is found to enhance the threshold of mPTP opening during reperfusion. The treatment with atractyloside stuck significantly the protection of heart of IPC in normal and OVX rat heart. These observations show that downregulation of GSK-3β through an impaired opening of mPTP during reperfusion and GSK-3β might be potential adjuvant to IPC against cardiac injury in OVX challenged rats.
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References
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