Effects of Thoracic Epidural Anesthesia on Cardiac Function and Myocardial Cell Apoptosis in Isoproterenol‐Induced Chronic Heart Failure Rats

Tao, Ge; Qin, Hao; Wang, Xu; Yang, Shuyan; Guo, Li; Han, Wei; Chang, Huiying

doi:10.1111/joic.12147

Cited by 6 publications

(5 citation statements)

References 41 publications

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“…Additionally, our results indicated that the HTEA + PDTC group showed no obvious myocardial infraction zone and decreased cell apoptosis rate, which indicated that inhibition of mTOR/NF-κB signaling pathway combined with HTEA reduced myocardial cell apoptosis. A study conducted by Ge et al (2014) once demonstrated that HTEA reduced myocardial cell apoptosis, decreased myocardial infraction size and myocardial abnormalities. Another previous study showed that mTOR/NF-κB signaling pathway could act as a mediator to influence cell apoptosis (Han, Zhang, Meng, Cheng, & Wang, 2016).…”

Section: Figurementioning

confidence: 99%

Retracted: Effects of mTOR/NF‐κB signaling pathway and high thoracic epidural anesthesia on myocardial ischemia‐reperfusion injury via autophagy in rats

Huang

Wen

Lin

et al. 2018

Journal Cellular Physiology

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We investigated the role of mammalian target of rapamycin/nuclear factor-kappa B (mTOR/NF-κB) signaling pathway in high thoracic epidural anesthesia (HTEA) against myocardial ischemia-reperfusion (I/R) injury in rats. The rat model of myocardial I/R injury was established. Ninety rats were divided into the normal, sham, I/R, eHTEA, the PDTC, and HTEA + PDTC groups. ELISA was applied to detect cardiac function indexes. HE staining was conducted to observe histopathological changes of myocardial tissues, and TTC staining was performed to detect the myocardial infarction size. TUNEL staining was adopted to detect the cell apoptosis rate. The mRNA and protein levels of mTOR, NF-κB, Fasl, Bcl-2 and Bax, and LC3-I, LC3-II, BNIP3, and Atg5 were detected by RT-qPCR and Western blotting, respectively. The findings indicated that compared with the normal and sham groups, the I/R, PDTC, and HTEA groups showed the larger myocardial infarction size and increased cell apoptosis rate, while the results in the HTEA + PDTC group were opposite. Compared with the normal and sham groups, the I/R group showed reduced mRNA and protein levels of Bcl-2, LC3, BNIP3, and Atg5, and elevated mRNA and protein levels of mTOR, p50, p65, Bax, and Fasl, while the HTEA + PDTC group revealed the opposite results, and the PDTC and HTEA group revealed the increased mRNA and protein levels of Bcl-2, LC3, BNIP3, Atg5, mTOR, p50, p65, Bax, and Fasl. These results prove that the inhibition of mTOR/NF-κB signaling pathway potentiates HTEA against myocardial IR injury by autophagy and apoptosis in rats.

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Section: Figurementioning

confidence: 99%

Retracted: Effects of mTOR/NF‐κB signaling pathway and high thoracic epidural anesthesia on myocardial ischemia‐reperfusion injury via autophagy in rats

Huang

Wen

Lin

et al. 2018

Journal Cellular Physiology

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“…Abnormal cell apoptosis is involved in the pathophysiological abnormalities of the cardiovascular system (Prescimone et al, 2013). The imbalance of apoptosis is related to the mechanism of many stress responses and the accumulation of myocardial apoptosis and the gradual decrease of cell numbers result in the incomplete development of heart function (Ge et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

USP49 inhibits ischemia–reperfusion‐induced cell viability suppression and apoptosis in human AC16 cardiomyocytes through DUSP1–JNK1/2 signaling

Zhang

et al. 2018

Journal Cellular Physiology

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Dual-specificity protein phosphatases (DUSP) also known as mitogen-activated protein kinase (MAPK) phosphatases (MKPs) can dephosphorylate MAPKs, including extracellular signal-regulated kinase, c-Jun N-terminal kinase (JNK), and p38. DUSP1-mediated JNK dephosphorylation has been found to play an antiapoptotic role against cardiac ischemia-reperfusion (I/R) injury. However, the regulation of DUSP1-JNK pathway remains unclear. In the current study, ubiquitin-specific peptidase 49 (USP49) expression in human AC16 cardiomyocytes following I/R injury was measured by real-time polymerase chain reaction and western blot analysis. Cell viability, apoptosis, the Bax, Bcl-2, and DUSP1 expression, and the activity of MAPKs in AC16 cardiomyocytes following indicated treatment was measured by CCK-8, flow cytometry, and western blot analysis. The direct interaction between USP49 and DUSP1 was measured by coimmunoprecipitation and ubiquitination analysis. The effect of USP49 on apoptosis and JNK activity in rat cardiomyocytes following I/R injury was also measured by TUNEL and western blot analysis. Here, we found that USP49 expression was time-dependently increased in AC16 cardiomyocytes following I/R. I/R-induced cell apoptosis and JNK1/2 activation both in in vivo and in vitro reversed by USP49 overexpression in AC16 cardiomyocytes. Inhibiting JNK1/2 activation significantly inhibited USP49 knockdown-induced the cell viability inhibition, apoptosis and the JNK1/2 activation in AC16 cardiomyocytes. Moreover, USP49 positively regulated DUSP1 expression through deubiquitinating DUSP1. Overall, our findings establish USP49 as a novel regulator of DUSP1-JNK1/2 signaling pathway with a protective role in cardiac I/R injury. K E Y W O R D S apoptosis, c-Jun N-terminal kinase 1/2, deubiquitination, dual-specificity protein phosphatases, ischemia-reperfusion J Cell Physiol. 2019;234:6529-6538.wileyonlinelibrary.com/journal/jcp

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“…MF can contribute to cardiac dysfunction in many pathophysiologic conditions [12]. The levels of LVED, LVES, LVEF and LVFS are main indexes of cardiac function [35]. This study showed that TPL improved cardiac dysfunction in MF rats.…”

Section: Discussionmentioning

confidence: 53%

Triptolide Inhibits the Activation of NLRP3 Inflammasome by Inhibiting NF-κB Pathway and Improves Myocardial Fibrosis

Shen

Wang

2021

Preprint

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ObjectiveTriptolide (TPL) is identified to be involved in the treatment for myocardial fibrosis (MF). This study investigated the mechanism of TPL in MF in rats and observed its effect on NLRP3 inflammasome signaling pathway.Materials and MethodsThe MF rat model was established by subcutaneous injection of isoproterenol (ISO), and treated by subcutaneous injection of TPL. After modeling for 1 week, the cardiac function of rats was evaluated, including LVEF, LVFS, LVES, LVED LVIDs and LVPWs. The HMI and LVMI were measured. The expressions of ANP, BNP, inflammatory related factors (IL-1β, IL-18, TNF-α, MCP-1, VCAM-1), and NLRP3 inflammasome factors (NLRP3, ASC, caspase-1) in rats were detected. HE staining and Masson staining were used to observe myocardial cell inflammation and fibrosis of rats.ResultsLVED, LVES, LVIDs and LVPWs of MF group were significantly upregulated, LVEF and LVFS were significantly downregulated, HMI and LVMI were upregulated, while TPL treatment reversed these trends; TPL treatment downregulated the tissue injury and improved the pathological damage of MF rats. TPL treatment downregulated the levels of inflammatory factors and fibrosis factors, and inhibited the activation of NLRP3 inflammasome. Activation of NLRP3 inflammasome or NF-κB pathway reversed the effect of TPL on MF.ConclusionsTPL inhibited the activation of NLRP3 inflammasome by inhibiting NF-κB pathway, and improved the degree of MF in MF rats.

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Effects of Thoracic Epidural Anesthesia on Cardiac Function and Myocardial Cell Apoptosis in Isoproterenol‐Induced Chronic Heart Failure Rats

Abstract: Our findings suggest that TEA may reduce myocardial apoptosis and decrease extent of structural damage and abnormalities in the myocardium.

Cited by 6 publications

References 41 publications

Retracted: Effects of mTOR/NF‐κB signaling pathway and high thoracic epidural anesthesia on myocardial ischemia‐reperfusion injury via autophagy in rats

Retracted: Effects of mTOR/NF‐κB signaling pathway and high thoracic epidural anesthesia on myocardial ischemia‐reperfusion injury via autophagy in rats

USP49 inhibits ischemia–reperfusion‐induced cell viability suppression and apoptosis in human AC16 cardiomyocytes through DUSP1–JNK1/2 signaling

Triptolide Inhibits the Activation of NLRP3 Inflammasome by Inhibiting NF-κB Pathway and Improves Myocardial Fibrosis

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