Protective Effect of Sevoflurane Postconditioning against Cardiac Ischemia/Reperfusion Injury via Ameliorating Mitochondrial Impairment, Oxidative Stress and Rescuing Autophagic Clearance

Yu, Peng; Zhang, Jing; Yu, Shuchun; Luo, Zhiqiang; Hua, Fuzhou; Yuan, Linhui; Zhou, Zhidong; Q, Liu; Du, Xiaohong; Chen, Sisi; Zhang, Lieliang; Xu, Guohai

doi:10.1371/journal.pone.0134666

Cited by 81 publications

(75 citation statements)

References 55 publications

(76 reference statements)

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“…It is widely known that in endogenous protection mechanisms, PC 16 and PostC 17 increase cell survival pathways, at least partially, by decreasing the oxidative stress damage after I/R injury [23][24][25][26]. Therefore it is interesting to review the role of the Trx system in the endogenous protection mechanisms.…”

Section: Thioredoxin Effects On Cardioprotection Mechanisms Ischemicmentioning

confidence: 99%

Role of thioredoxin-1 in ischemic preconditioning, postconditioning and aged ischemic hearts

D'Annunzio

Pérez

Boveris

et al. 2016

Pharmacological Research

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Section: Thioredoxin Effects On Cardioprotection Mechanisms Ischemicmentioning

confidence: 99%

Role of thioredoxin-1 in ischemic preconditioning, postconditioning and aged ischemic hearts

D'Annunzio

Pérez

Boveris

et al. 2016

Pharmacological Research

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“…Sevoflurane is a widely used volatile anesthetic in cardiac surgery. It is demonstrated that sevoflurane postconditioning (SPC) limits myocardial infarct size and reduces mortality in both animal models and clinical practice [3][4][5][6]. Similarly, remote ischemic preconditioning (RIPC) by applying several cycles of ischemia and reperfusion in distant tissues also presents the protective effect.…”

Section: Introductionmentioning

confidence: 99%

“…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%

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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“…Several studies suggest that sevoflurane exposure induces neuroapoptosis through caspase-3 activation and increase in β-amyloid protein levels in vivo and in vitro, while other studies suggest a neuroprotective effect [29] [30] [31]. This discrepancy could be explained by differences in cells lines, exposure time to anesthesia and concentration of inhalation agents.…”

Section: Discussionmentioning

confidence: 99%

Evaluation of Stress Response and Apoptosis on Leucocytes in TIVA versus Balanced Anesthesia

Soto¹,

Pignolo²,

Calero³

et al. 2017

OJApo

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Background: The aim of this study was to assess the stress response and apoptosis on leucocytes, in patients under two different anesthetics techniques. Methods: Thirty patients ASA I-II were prospectively randomized into two groups to receive either total intravenous anesthesia with propofolremifentanil (TIVA Group, n = 15) or balanced inhalation anesthesia with sevoflurane-remifentanil (BAL Group, n = 15). The hemodynamic response: systolic blood pressure (SBP), diastolic blood pressure (DBP) and heart rate (HR) at different time points: baseline, after intubation, after skin incision and at the end of surgery, was measured along with plasma levels of lactate, glucose, cortisol and leucocytes count. The biomarkers of apoptosis (Annexin V and Propidium Iodide) in neutrophils, monocytes and lymphocytes were evaluated at baseline, intraoperatively and two hours after surgery. Results: The study groups were comparable with respect to anthropometric data. No significant intergroup differences in SBP and DBP were revealed. The HR in the BAL group was lower after intubation (p = 0.007). In both groups, lactate, plasma glucose, cortisol and leucocytes count remained stable during surgery and two hours post-operatively. In the BAL group there were significant differences in Annexin V in neutrophils, baseline moment (p = 0.010). No significant differences were found in apoptosis markers (Annexin V and Propidium Iodide) in neutrophils, monocytes and lymphocytes, at different time points. Conclusion: Both TIVA and BAL were effective in suppressing the surgical stress, without inducing apoptosis in immune cells, in patients undergoing VCL.

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Protective Effect of Sevoflurane Postconditioning against Cardiac Ischemia/Reperfusion Injury via Ameliorating Mitochondrial Impairment, Oxidative Stress and Rescuing Autophagic Clearance

Cited by 81 publications

References 55 publications

Role of thioredoxin-1 in ischemic preconditioning, postconditioning and aged ischemic hearts

Role of thioredoxin-1 in ischemic preconditioning, postconditioning and aged ischemic hearts

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

Evaluation of Stress Response and Apoptosis on Leucocytes in TIVA versus Balanced Anesthesia

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