Sevoflurane Postconditioning Reduces Hypoxia-Reoxygenation Injury in H9C2 Embryonic Rat Cardiomyocytes and Targets the STRADA Gene by Upregulating microRNA-107

Jiang, Qun; Gu, Shan Zhi

doi:10.12659/msm.920849

Cited by 5 publications

(5 citation statements)

References 43 publications

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“…Also, our conclusion was consistent with Yu et al, who described that the cardiomyocyte apoptosis inhibited by sevoflurane postconditioning may influence the modulation of the expression of pro-and antiapoptotic proteins, specifically Bcl-2, BAX, and phosphor-Bad [26]. Besides, the study has indicated that sevoflurane could significantly improve the hypoxiareoxygenation injury of the rats via decreasing the apoptosis of cardiomyocytes [27].…”

Section: Discussionsupporting

confidence: 92%

[Retracted] Effects of Sevoflurane on Apoptosis of Myocardial Cells in IRI Rats

Zhang

et al. 2021

BioMed Research International

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Background. Cardiomyocyte apoptosis functions essentially in ischemia/reperfusion- (I/R-) induced myocardial injury. It is suggested that autophagy is widely implicated in the regulation of cell survival and death. Sevoflurane, as a largely used inhalational general anesthetic, has been shown to have a protective effect on cardiomyocytes. However, it was yet elusive on the underlying mechanisms. Aim. The objective of this study is to investigate the association of sevoflurane-mediated cardioprotective effects with autophagy regulation. Methods. An in vitro hypoxia model was established in primary cardiomyocytes from fresh myocardial tissue of the rats. The apoptosis rate of myocardial cells treated with hypoxia and treated with sevoflurane was measured. Western blot and immunocytochemical assay were used to measure the protein expression. The cell proliferation rate and cell apoptosis were measured using the MTT assay and flow cytometry, respectively. Results. The expression of apoptotic proteins including B cell lymphoma-2 (Bcl-2), CCAAT/enhancer-binding protein homologous protein (CHOP), glucose-regulated protein 78 (GRP78), and Bcl-2-associated X protein (BAX) in myocardium treated with sevoflurane was significantly lower than that in myocardium treated with hypoxia. The expression of adhesion proteins such as intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and E-selectin in myocardium treated with sevoflurane was higher than that in myocardium treated with hypoxia, suggesting better connectivity of the myocardium. Conclusion. Sevoflurane treatment reduced the apoptosis of myocardial cells after hypoxia treatment.

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Section: Discussionsupporting

confidence: 92%

[Retracted] Effects of Sevoflurane on Apoptosis of Myocardial Cells in IRI Rats

Zhang

et al. 2021

BioMed Research International

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“…Subsequently, H9c2 cells were transfected with miR-107 mimics, and we observed the same shift in TNF-α and IL-6 levels as in in vivo experiments. A report indicated that the H9c2 cell proliferation was evidently increased and cell apoptosis was inhibited after transfection with miR-107 mimic [Jiang and Gu, 2020]. Consistently, our findings demonstrated that miR-107 overexpression increased LPS-induced cardiomyocyte proliferation, inhibited apoptosis, and enhanced the proportion of cardiomyocytes arrested in S and G2/M phases.…”

Section: Discussionsupporting

confidence: 90%

“…Then, the RT-qPCR test validated that miR-107 expression in rat serum of the CLP group was significantly decreased. The expression of miR-107 has been reported to have an important role in the myocardial necrosis [Jiang and Gu, 2020]. To explore the effect of miR-107 in sepsis-induced myocardial injury, the sepsis rats were injected with adenovirus vectors that expressed miR-107-mimics through tail veins.…”

Section: Discussionmentioning

confidence: 99%

miR-107 Attenuates Sepsis-Induced Myocardial Injury by Targeting PTEN and Activating the PI3K/AKT Signaling Pathway

Zhang¹,

Li²,

Li³

et al. 2022

Cells Tissues Organs

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Sepsis is a public health problem worldwide. This study investigated the mechanism of miR-107 on sepsis-induced myocardial injury. Sepsis rat models were established by cecal ligation and puncture, and the cell model was established using lipopolysaccharide (LPS)-induced cardiomyocytes. Cardiac function indexes of rats were measured using echocardiography. Pathological changes in the rat myocardium were observed using histological staining. Expressions of miR-107 in the serum of rats and cardiomyocyte were detected after the treatment of miR-107 mimic or/and pcDNA3.1-PTEN, followed by assessment of cell cycle, proliferation, and apoptosis. Binding sites of miR-107 and PTEN were predicted. PTEN, PI3K, p-PI3K, AKT, and p-AKT expressions in LPS-induced cardiomyocytes were measured. miR-107 was significantly downregulated in the serum of CLP rats and LPS-induced cardiomyocytes. miR-107 overexpression remarkably improved cardiac function and histological changes, decreased inflammatory factors, and alleviated the sepsis-induced myocardial injury in rats. In LPS-induced cardiomyocytes, miR-107 overexpression increased cardiomyocyte proliferation, inhibited apoptosis, and enhanced the proportion of cardiomyocytes arrested in S and G2/M phases. miR-107 targeted PTEN. PTEN overexpression partially reversed the inhibition of miR-107 mimic on cardiomyocyte apoptosis. miR-107 overexpression activated the PI3K/AKT pathway by inhibiting PTEN. To conclude, miR-107 activates the PI3K/AKT pathway by inhibiting PTEN, thus attenuating sepsis-induced myocardial injury and LPS-induced cardiomyocyte apoptosis.

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“…Then, cells were divided into four groups: a model group (M), single sevoflurane treatment group (S), sevoflurane treatment combined with NLRC3 overexpression group (O), and a sevoflurane treatment combined with NLRC3 inhibition group (I). In the sevoflurane treatment group, cells were treated with 2.4% (v/v) sevoflurane for 20 min at the end of ischaemia reperfusion model construction [14].…”

Section: Methodsmentioning

confidence: 99%

Overexpression of NLRC3 enhanced inhibition effect of sevoflurane on inflammation in an ischaemia reperfusion cell model

Li¹,

Hu²,

Xu³

2020

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Brain ischaemia is one of the leading causes of mortality and disability worldwide, and the damage caused by ischaemia not only induces primary damage but also that induced by ischaemia-reperfusion (I/R) injury. Multiple processes including inflammation and oxidative stress response play important roles in the development of brain ischaemia injury. Sevoflurane is a well-known volatile anaesthetic, and a recent study discovered the role of sevoflurane in suppression of the inflammation response process via inhibition of inflammatory infiltrates and production, maintaining the balance of cytokine responses, although the possible mechanism was not fully clear. NLRC3 is a member of the nucleotide-binding domain and leucine-rich repeat containing (NLR) family, and it has been regarded as a regulator of the inflammation process via the regulation of inflammasome formation, which is an initiator of inflammatory events. In the present study, we found that overexpression of NLRC3 reduced the apoptosis in a cellular model of ischaemia reperfusion, and the expression of pro-inflammatory cytokines was also decreased. Further study found that these effects might be mediated by the TRAF6/TLR4/NF-κB signalling pathway. Thus, we speculate that overexpression might enhance the effect of sevoflurane in inhibiting the inflammatory response process in an ischaemia reperfusion model, which might be a new therapeutic strategy.

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Sevoflurane Postconditioning Reduces Hypoxia-Reoxygenation Injury in H9C2 Embryonic Rat Cardiomyocytes and Targets the STRADA Gene by Upregulating microRNA-107

Cited by 5 publications

References 43 publications

[Retracted] Effects of Sevoflurane on Apoptosis of Myocardial Cells in IRI Rats

[Retracted] Effects of Sevoflurane on Apoptosis of Myocardial Cells in IRI Rats

miR-107 Attenuates Sepsis-Induced Myocardial Injury by Targeting PTEN and Activating the PI3K/AKT Signaling Pathway

Overexpression of NLRC3 enhanced inhibition effect of sevoflurane on inflammation in an ischaemia reperfusion cell model

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