Sufentanil postconditioning protects the myocardium from ischemia-reperfusion via PI3K/Akt-GSK-3β pathway

Wu, Qiaoling; Tu, Shen; Ma, Hong; Wang, Junke

doi:10.1016/j.jss.2012.05.081

Cited by 38 publications

(29 citation statements)

References 38 publications

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“…Then many researches paid attention on the role of GSK-3β on myocardial protection. Recent studies have found that GSK-3β is where cardiomyocyte damage and eventually death converge in the process of myocardial ischemia and phosphorylation of GSK-3β is crucial in multiple cardioprotective signaling pathways (18)(19)(20). But the downstream mechanism is unclear.…”

Section: Discussionmentioning

confidence: 99%

“…Since then, much attention has been paid to its role in inflammatory diseases. Moreover, previous works have shown that much endogenous and exogenous cardioprotection plays efficacy by depressing the activation of GSK-3β (18)(19)(20), whereas the precise downstream mechanism is unclear. Mitochondrial permeability transition pore (mPTP) is a nonselective high conductance channel between the inner and outer membranes of the mitochondria.…”

mentioning

confidence: 99%

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Glycogen Synthase Kinase 3β Inhibition Protects the Cardiomyocytes from Anoxia/Reoxygenation Injury by Modulating Inﬂammatory Response and Reducing the Opening of mPTP

Cheng¹,

Jun²,

Xue³

et al. 2015

J Anesth Perioper Med

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Background: Phosphorylation of glycogen synthase kinase 3β (GSK-3β) is crucial in multiple cardioprotective signaling pathways. But the downstream mechanism is unclear. Considering GSK-3β is the key regulator of nuclear factor-κB (NF-κB) and mitochondrial permeability transition pore (mPTP) is a critical determinant of lethal reperfusion injury, we assessed the mechanism of postconditioning with the selective inhibitor of GSK-3β associated with modulating in fl ammatory response and reducing the opening of mPTP. Methods: After cultured for 72 hours, neonatal rat cardiomyocytes were randomly divided into 3 groups according to random number table: Sham group, anoxia/reoxygenation injury group (AR group) and GSK-3β inhibitor TDZD -8 postconditioning group (TDZD -8 group). At the end of the experiment, the lactate dehydrogenase (LDH) release rate, myocardial apoptosis and the supernatant concentrations of interleukin (IL)-6 and tumor necrosis factor (TNF)-α were measured. The NF-κBp65 and phosphorylated NF-κBp65Ser536 in all samples were assessed by western-blotting technique. The mitochondrial membrane potential was measured by rhodamine 123 staining flow cytometry and confocal laser scanning microscope. Results: We discovered that postconditioning with GSK-3β inhibitor TDZD -8 could significantly protect against cardiomyocyte anoxia/reoxygenation injury, as shown by reducing the early apoptosis and LDH release rate. And this cardioprotective method could significantly attenuate inflammatory response to the anoxia/reoxygenation injury, as evidenced by decreasing the activity of NF-κB and levels of inflammatory cytokines, such as IL-6 and TNF-α. Furthermore, it could significantly reduce the irreversibly high level opening of the mPTP, as evidenced by increasing the mitochondrial membrane potential of anoxia/reoxygenation cardiomyocyte. Conclusions: Our current results indicated that postconditioning with GSK-3β inhibitor TDZD -8 significantly attenuated the systemic inflammatory and reduced the opening of mPTP response to cardiomyocytes anoxia/reoxygenation injury.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Glycogen Synthase Kinase 3β Inhibition Protects the Cardiomyocytes from Anoxia/Reoxygenation Injury by Modulating Inﬂammatory Response and Reducing the Opening of mPTP

Cheng¹,

Jun²,

Xue³

et al. 2015

J Anesth Perioper Med

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“…Tsang et al (36) showed that ischemic postconditioning increased phosphorylation of Akt and inhibition of Akt activity partly abolished the cardioprotective effects of ischemic postconditioning. Many cardioprotectants, including erythropoietin (4), sulfentanil (17), and KB-R7943 (37), confer their cardioprotective effects through the PI3K/Akt pathway. In this study, Que postconditioning significantly increased phosphorylation of Akt and reduced cardiomyocyte apoptosis by regulating the Bcl-2 family.…”

Section: Discussionmentioning

confidence: 99%

“…The in vivo myocardial I/R model was modified from a previous study (17). Briefly, rats were anesthetized by an intraperitoneal ( ip ) injection of 40 mg/kg 1% pentobarbital sodium.…”

Section: Methodsmentioning

confidence: 99%

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Quercetin postconditioning attenuates myocardial ischemia/reperfusion injury in rats through the PI3K/Akt pathway

Wang

Zhang

et al. 2013

Braz J Med Biol Res

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Quercetin (Que), a plant-derived flavonoid, has multiple benefical actions on the cardiovascular system. The current study investigated whether Que postconditioning has any protective effects on myocardial ischemia/reperfusion (I/R) injury in vivo and its potential cardioprotective mechanisms. Male Sprague-Dawley rats were randomly allocated to 5 groups (20 animals/group): sham, I/R, Que postconditioning, Que+LY294002 [a phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathway inhibitor], and LY294002+I/R. I/R was produced by 30-min coronary occlusion followed by 2-h reperfusion. At the end of reperfusion, myocardial infarct size and biochemical changes were compared. Apoptosis was evaluated by both TUNEL staining and measurement of activated caspase-3 immunoreactivity. The phosphorylation of Akt and protein expression of Bcl-2 and Bax were determined by Western blotting. Que postconditioning significantly reduced infarct size and serum levels of creatine kinase and lactate dehydrogenase compared with the I/R group (all P<0.05). Apoptotic cardiomyocytes and caspase-3 immunoreactivity were also suppressed in the Que postconditioning group compared with the I/R group (both P<0.05). Akt phosphorylation and Bcl-2 expression increased after Que postconditioning, but Bax expression decreased. These effects were inhibited by LY294002. The data indicate that Que postconditioning can induce cardioprotection by activating the PI3K/Akt signaling pathway and modulating the expression of Bcl-2 and Bax proteins.

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Eupatilin: Sources, Extraction, Derivatives, and Pharmacological Activity

Malhotra,

Ashri,

Singla

et al. 2023

Handbook of Dietary Flavonoids

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Sufentanil postconditioning protects the myocardium from ischemia-reperfusion via PI3K/Akt-GSK-3β pathway

Cited by 38 publications

References 38 publications

Glycogen Synthase Kinase 3β Inhibition Protects the Cardiomyocytes from Anoxia/Reoxygenation Injury by Modulating Inﬂammatory Response and Reducing the Opening of mPTP

Glycogen Synthase Kinase 3β Inhibition Protects the Cardiomyocytes from Anoxia/Reoxygenation Injury by Modulating Inﬂammatory Response and Reducing the Opening of mPTP

Quercetin postconditioning attenuates myocardial ischemia/reperfusion injury in rats through the PI3K/Akt pathway

Eupatilin: Sources, Extraction, Derivatives, and Pharmacological Activity

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