indirubin/infarction

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Cardioprotective effect of indirubin in experimentally induced myocardial infarction in wistar rats.

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Recently, there has been as enhanced interest on global level to recognize the potent antioxidant compounds which are pharmacologically active with less or no side effects. Thus, the current investigation was intended to scrutinize the protective effect of indirubin on the cardiac marker, such as,

Gsk-3β inhibitors mimic the cardioprotection mediated by ischemic pre- and postconditioning in hypertensive rats.

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The aim of this study was to examine the effects of GSK-3 β inhibitors compared with PRE and POS in spontaneously hypertensive rats (SHR). Isolated hearts were submitted to the following protocols: IC: 45 min global ischemia (GI) and 1-hour reperfusion (R); PRE: a cycle of 5 min GI and 10 minutes of

Modulation of the cardioprotective effect of ischemic preconditioning in hyperlipidaemic rat heart.

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Ischemic preconditioning (IPC) produces cardioprotection by phosphorylation of glycogen synthaes kinase-3beta (GSK-3beta) that inhibits the opening of mitochondrial permeability transition pore (MPTP), and this cardioprotective action of IPC is attenuated by hyperlipidaemia. The present study

Involvement of GSK-3β in attenuation of the cardioprotective effect of ischemic preconditioning in diabetic rat heart.

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Ischemic preconditioning (IPC) produces cardioprotection by phosphorylation of glycogen synthase kinase-3β (GSK-3β) that inhibits the opening of mitochondrial permeability transition pore (MPTP). The activity of glycogen GSK-3β is elevated during diabetes mellitus (DM). This study investigated the

Pharmacological inhibition of GSK-3β produces late phase of cardioprotection in hyperlipidemic rat: possible involvement of HSP 72.

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The acute, as well as late, phase of cardioprotection induced by ischemic preconditioning is abolished in hyperlipidemic (HL) rat heart. The pharmacological inhibition of glycogen synthase kinase-3β (GSK-3β), has earlier been reported to restore this attenuated acute cardioprotective effect.

Meisoindigo Protects Against Focal Cerebral Ischemia-Reperfusion Injury by Inhibiting NLRP3 Inflammasome Activation and Regulating Microglia/Macrophage Polarization via TLR4/NF-κB Signaling Pathway.

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Ischemic stroke is a devastating disease with long-term disability. However, the pathogenesis is unclear and treatments are limited. Meisoindigo, a second-generation derivative of indirubin, has general water solubility and is well-tolerated. Previous studies have shown that meisoindigo reduces

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