The effect of sevoflurane postconditioning on cardioprotection against ischemia-reperfusion injury in rabbits

Dong, Chen; Cheng, Bo; Zhou, Haiyan; Li, Lihuan

doi:10.1007/s11033-011-1419-5

Cited by 12 publications

(6 citation statements)

References 21 publications

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“…The sample size was chosen according to the previous studies by our group. [ 10 12 ] Data were expressed as mean ± standard deviation (SD). The variables of LV contractile function were analyzed using two-way analysis of variance (ANOVA).…”

Section: Ethodsmentioning

confidence: 99%

“…Numerous studies have concerned about the mechanisms of these two noninvasive approaches. [ 7 8 9 10 ] Currently, it is believed that both SevoPoC and early RIPC could activate reperfusion injury salvage kinase (RISK) pathway, comprising phosphoinositide 3-kinase-protein kinase B/Akt and extracellular signal-regulated kinase 1 and 2, and Survivor Activating Factor Enhancement (SAFE) such as STAT3. [ 11 12 13 14 ] However, there is little information on the mechanisms responsible for the cardioprotection by delayed remote ischemic preconditioning (DRIPC).…”

Section: Introductionmentioning

confidence: 99%

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Downregulation of Na+/Ca2+ Exchanger Isoform 1 Protects Isolated Hearts by Sevoflurane Postconditioning but Not by Delayed Remote Ischemic Preconditioning in Rats

Zhou

Yao

et al. 2017

Chinese Medical Journal

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Background:Calcium regulatory proteins-L-type Ca2+ channels (LTCCs), ryanodine receptor 2 (RyR2), and Na+/Ca2+ exchanger isoform 1 (NCX1) have been recognized as important protective mechanisms during myocardial ischemia-reperfusion injury (I/RI). Both sevoflurane postconditioning (SevoPoC) and delayed remote ischemic preconditioning (DRIPC) have been shown to protect the heart against I/RI. In this study, we aimed to compare the effects of SevoPoC and DRIPC on the expression of the three calcium regulatory proteins in an isolated rat heart model.Methods:After 30-min balanced perfusion, isolated hearts from rats were subjected to 30-min ischemia followed by 60-min reperfusion. Totally 40 isolated hearts were randomly assigned to four groups (n = 10/group): time control group, I/RI group, SevoPoC group, and DRIPC group. The effect of SevoPoC (3% v/v) and DRIPC were observed. Myocardial infarct size (IS), cardiac troponin I level, and heart function were measured. The protein and messenger RNA levels of LTCCs, RyR2, and NCX1 were determined.Results:Both SevoPoC and DRIPC improved the recovery of myocardial function, and reduced cardiac troponin I release after I/RI. The decrease in IS was more significant in the SevoPoC group than that in the DRIPC group (16.50% ± 4.54% in the SevoPoC group [P = 0.0006], and 22.34% ± 4.02% in the DRIPC group [P = 0.0007] vs. 35.00% ± 5.24% in the I/RI group, respectively). SevoPoC, but not DRIPC significantly inhibited the activity of NCX1 (0.59 ± 0.09 in the I/RI group vs. 0.32 ± 0.16 in the SevoPoC group, P = 0.006; vs. 0.57 ± 0.14 in the DRIPC group, P = 0.072). No statistical significant differences were observed in the expression of LTCCs and RyR2 between SevoPoC and DRIPC. In addition, subsequent correlation analysis showed a significantly positive relationship between the cardiac troponin I level and the protein expression of NCX1 (r = 0.505, P = 0.023).Conclusion:SevoPoC may be more effective in the cardioprotection than DRIPC partly due to the deactivation of NCX1.

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Section: Ethodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Downregulation of Na+/Ca2+ Exchanger Isoform 1 Protects Isolated Hearts by Sevoflurane Postconditioning but Not by Delayed Remote Ischemic Preconditioning in Rats

Zhou

Yao

et al. 2017

Chinese Medical Journal

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“…And recent researches have confirmed that inhibiting mPTP opening at reperfusion could protect against IRI (38,39). Furthermore, it is thought that mPTP is the ultimate determinant of myocardial cell apoptosis (21)(22)(23) and it is the key mechanism of many different types of cardioprotective methods (24)(25)(26)(27). So we speculated the mechanism of cardioprotection from the inhibitor of GSK-3β which is highly possible associated with reducing the irreversibly high level opening of mPTP and activating the apoptotic pathways in turn that aggravates myocardial IRI.…”

Section: Discussionmentioning

confidence: 99%

“…The high level irreversible opening of mPTP is another important mechanism of IRI. Past and recent researches definitely established that mPTP is the ultimate determinant of myocardial cell apoptosis (21)(22)(23) and it is the key mechanism of many different types of cardioprotective methods, such as preconditioning, postconditioning and some pharmacological postconditioning (24)(25)(26)(27).…”

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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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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“…Data on the cardioprotective properties of NIM811 were confirmed in 2012 through the use of the isolated heart I/R model in rats with streptozotocin‐induced diabetes (Sloan et al, ). Chen, Cheng, Zhou, and Li () found that the mPTP inhibitor NIM811 reduces the infarct size in vivo and decreases the plasma level of troponin I in rabbits at reperfusion, followed after 15 or 30 min, but not 60 min coronary occlusion.…”

Section: Experimental Studies On the Cardioprotective Activity Of Mptmentioning

confidence: 99%

Pharmacology of mitochondrial permeability transition pore inhibitors

Naryzhnaya

Маслов

Oeltgen

2019

Drug Development Research

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It is now firmly established that an important event in the formation of reperfusion injury of the heart is the opening of mitochondrial permeability transition pores (mPTPs), which changes the permeability of the mitochondria. mPTP opening results in the death of cardiomyocytes through activation of apoptosis and necroptosis. Experimental studies have shown that pharmacological inhibition of mPTP opening promotes the reduction in the infarct size and the suppression of apoptosis. Indeed, studies have shown the efficacy of mPTP inhibitors in animal models of myocardial reperfusion and isolated human myocardial trabeculae. However, clinical trials of cyclosporin A and TRO40303 have not provided a clear answer to the question of the effectiveness of mPTP inhibitors in patients with acute myocardial infarction. This article presents an analysis of possible approaches for the pharmacological regulation of mPTP during reperfusion injury of the heart.

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The effect of sevoflurane postconditioning on cardioprotection against ischemia-reperfusion injury in rabbits

Cited by 12 publications

References 21 publications

Downregulation of Na+/Ca2+ Exchanger Isoform 1 Protects Isolated Hearts by Sevoflurane Postconditioning but Not by Delayed Remote Ischemic Preconditioning in Rats

Downregulation of Na+/Ca2+ Exchanger Isoform 1 Protects Isolated Hearts by Sevoflurane Postconditioning but Not by Delayed Remote Ischemic Preconditioning in Rats

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

Pharmacology of mitochondrial permeability transition pore inhibitors

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