Sevoflurane Postconditioning Protects Chronically-Infarcted Rat Hearts against Ischemia-Reperfusion Injury by Activation of Pro-survival Kinases and Inhibition of Mitochondrial Permeability Transition Pore Opening upon Reperfusion

Yao, Yun-Tai; Li, Lihuan; Li, Libing; Gao, Changqing; Shi, Chunxia

doi:10.1248/bpb.32.1854

Cited by 40 publications

(37 citation statements)

References 53 publications

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“…Postconditioning with sevoflurane reduced myocardial apoptosis induced by I/R via multiple mechanisms, such as preventing activation of caspase 3/9 [18], and inhibiting the opening of mitochondrial permeability transition pore (mPTP) [9]. Clinical research uncovered that the molecular mechanisms of sevoflurane protection include its anti-inflammatory effects [19], which was consistent with our present finding.…”

Section: Discussionsupporting

confidence: 91%

“…Nevertheless, the combined effect is not tested in rat myocardial ischemia/reperfusion (I/R) model. Previous studies suggest that a variety of mechanisms may be responsible for the cardioprotection of SPC and RIPC against I/R injury, including the Reperfusion Injury Salvage Kinase pathway (RISK pathway) inhibition [8], preventing mitochondrial permeability transition pore (mPTP) from opening [9], decreasing intracellular reactive oxygen species (ROS) levels [10], and regulating the activation of autophagy or the process of autophagic flux [4,11]. However, the precise mechanisms remain unclear.…”

Section: Introductionmentioning

confidence: 99%

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Remote Ischaemic Preconditioning and Sevoflurane Postconditioning Synergistically Protect Rats from Myocardial Injury Induced by Ischemia and Reperfusion Partly via Inhibition TLR4/MyD88/NF-κB Signaling Pathway

Zhang

et al. 2017

Cell Physiol Biochem

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Background/Aims: A combination sevoflurane postconditioning (SPC) and remote ischemic preconditioning (RIPC) is proved effective in an ex vivo rat heart perfusion model. However, the combined effect of those two interventions is not tested in rat myocardial ischemia/reperfusion (I/R) model, and the underlying mechanisms remain to be elucidated. This study aimed to investigate the effect in vivo using a rat myocardial I/R model and illuminate the related mechanisms. Methods: Forty male Sprague-Dawley rats were randomly divided into the following 5 groups: i) sham-operated control; ii) I/R; iii) I/R + RIPC; iv) I/R + SPC; v) I/R + RIPC + SPC. The hemodynamic parameters were recorded at the end of reperfusion. The histological changes including the infarct size were assessed using Triphenyltetrazolium chloride (TTC) staining and H&E staining. In addition, the circulating levels of cardiac enzymes (CK-MB, hs-cTnT, and cTnT) inflammatory cytokines (IL-6, IL-8, and TNF-α) were detected. The expression levels of apoptosis-related proteins (C-Caspase 3, PARP, Bax, and Bcl-2), proinflammatory factors (TLR4, HMGB-1, MyD88, and p65), and IKB-α were measured by Western blot analysis. Real-time PCR was performed to detect mRNA levels of the proinflammatory factors. Results: Both SPC and RIPC significantly reduced the infarct size, cardiac enzyme release, inflammatory cytokine secretion, and proinflammatory factor expression, and increased IKB-α expression compared to I/R group. Furthermore, the combination of those two strategies had synergic infarct size limiting and anti-inflammatory effects. Conclusions: The finding of this study suggested that the combination of SPC and RIPC had a potentially cardioprotective effect through inhibiting TLR4/MyD88/NF-κB signaling.

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Section: Discussionsupporting

confidence: 91%

Section: Introductionmentioning

confidence: 99%

Remote Ischaemic Preconditioning and Sevoflurane Postconditioning Synergistically Protect Rats from Myocardial Injury Induced by Ischemia and Reperfusion Partly via Inhibition TLR4/MyD88/NF-κB Signaling Pathway

Zhang

et al. 2017

Cell Physiol Biochem

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“…Several lncRNAs are dysregulated during acute myocardial infarction or heart failure, whereas others could control hypertrophy, mitochondrial function and cardiomyocyte apoptosis, and identified cardiovascular lncRNAs might play significant roles in cardiovascular diseases [36]. Previous studies have indicated that sevoflurane postconditioning could protect isolated mouse hearts against I/R injury [9,37]. A previous study showed that cAMP/PKA activation as a regulator could halt pathological cell recruitment, prevent destructive immune reactions, and promote hepatocyte survival, which might raise defensive thresholds to inflammatory responses [34].…”

Section: Discussionmentioning

confidence: 99%

Suppression of Long Non-Coding RNA LINC00652 Restores Sevoflurane-Induced Cardioprotection Against Myocardial Ischemia-Reperfusion Injury by Targeting GLP-1R Through the cAMP/PKA Pathway in Mice

Zhang

Liu

et al. 2018

Cell Physiol Biochem

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Background/Aims: Long non-coding RNA (lncRNA) and glucagon-like peptide 1 receptor (GLP-1R) are crucial for heart development and for adult heart structural maintenance and function. Herein, we performed a study to explore the effect of lncRNA LINC00652 (LINC00652) on myocardial ischemia-reperfusion (I/R) injury by targeting GLP-1R through the cyclic adenosine monophosphate-protein kinase A (cAMP/PKA) pathway. Methods: Bioinformatics software was used to screen the long-chain non-coding RNAs associated with myocardial ischemia-reperfusion and to predict target genes. The mRNA and protein levels of LINC00652, GLP-1R and CREB were detected by RT-qPCR and western blotting. In order to identify the interaction between LINC00652 and myocardial I/R injury, the cardiac function, the hemodynamic changes, the pathological changes of the myocardial tissues, the myocardial infarct size, and the apoptosis of myocardial cells of mice were measured. Meanwhile, the levels of serum IL-1β and TNF-α were detected. Results: LINC00652 was overexpressed in the myocardial cells of mice with myocardial I/R injury. GLP-1R is the target gene of LINC00652. We also determined higher levels of LINC00652 and GLP-1R in the I/R modeled mice. Additionally, si-LINC00652 decreased cardiac pathology, infarct size, apoptosis rates of myocardial cells, and levels of IL-1β and TNF-α, and increased GLP-1R expression cardiac function, normal hemodynamic index, and the expression and phosphorylation of GLP-1R and CREB proteins. Conclusion: Taken together, our key findings of the present highlight LINC00652 inhibits the activation of the cAMP/PKA pathway by targeting GLP-1R to reduce the protective effect of sevoflurane on myocardial I/R injury in mice.

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“…For example, the JAK-STAT pathway plays an essential role in development of ischemic preconditioning-induced cardioprotection [190][191][192][193]. Protein kinase B/Akt [194][195][196] and protein kinase C (PKC) signaling [197][198][199][200][201][202][203][204][205] are implicated in protection against myocardial ischemic injury. Recent studies have proposed a comprehensive view of the reperfusion injury salvage kinase (RISK) pathway [206], which connects pro-survival (PI3K)-Akt and the p42 (ERK1/2) signaling, thus mediating the cardioprotection provided by ischemic and pharmacological preconditioning [207,208].…”

Section: Protein Phosphorylation and Cardiac Diseasesmentioning

confidence: 99%

Phosphoproteomics and molecular cardiology: Techniques, applications and challenges

Sun

Hamilton

Reardon

2012

Journal of Molecular and Cellular Cardiology

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Sevoflurane Postconditioning Protects Chronically-Infarcted Rat Hearts against Ischemia-Reperfusion Injury by Activation of Pro-survival Kinases and Inhibition of Mitochondrial Permeability Transition Pore Opening upon Reperfusion

Cited by 40 publications

References 53 publications

Remote Ischaemic Preconditioning and Sevoflurane Postconditioning Synergistically Protect Rats from Myocardial Injury Induced by Ischemia and Reperfusion Partly via Inhibition TLR4/MyD88/NF-κB Signaling Pathway

Remote Ischaemic Preconditioning and Sevoflurane Postconditioning Synergistically Protect Rats from Myocardial Injury Induced by Ischemia and Reperfusion Partly via Inhibition TLR4/MyD88/NF-κB Signaling Pathway

Suppression of Long Non-Coding RNA LINC00652 Restores Sevoflurane-Induced Cardioprotection Against Myocardial Ischemia-Reperfusion Injury by Targeting GLP-1R Through the cAMP/PKA Pathway in Mice

Phosphoproteomics and molecular cardiology: Techniques, applications and challenges

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