Electroacupuncture Pretreatment Regulates Apoptosis of Myocardial Ischemia-Reperfusion Injury in Rats Through RhoA/p38MAPK Pathway Mediated by miR-133a-5p

Han, Yongli; Chen, Song; Wang, Hua

doi:10.1155/2021/8827891

Cited by 8 publications

(6 citation statements)

References 27 publications

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“…e pathophysiological mechanism of myocardial ischemia-reperfusion injury is complex. Studies have shown that myocardial ischemia can promote in ammation and oxidative stress translation and can lead to myocardial apoptosis through reperfusion, in which inammatory factors can activate and chemotaxis leukocytes, which are also the products of activation of the leukocytes, which can aggravate myocardial injury [1,[7][8][9]. Superoxide dismutase (SOD) is essential to prevent oxidative stress, and it can e ectively resist the damage of oxygen free radicals to the body through its antioxidant and antifree radical functions [10].…”

Section: Introductionmentioning

confidence: 99%

Paeoniflorin Protects H9c2 Cardiomyocytes against Hypoxia/Reoxygenation Induced Injury via Regulating the AMPK/Nrf2 Signaling Pathway

Sun

Tan

et al. 2022

Evidence-Based Complementary and Alternative Medicine

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Myocardial ischemia/reperfusion (MIR) injury contributes to the exacerbation of heart disease by causing cardiac arrhythmias, myocardial infarction, and even sudden death. Studies have found that paeoniflorin (PF) has a protective effect on coronary artery disease (CAD). However, the mechanism of PF in MIR has not been fully investigated. The purpose of this study was to investigate the functional role of PF in H9c2 cells subjected to hypoxia/reoxygenation (H/R). Here, PF treatment enhanced cell viability in H/R-stimulated H9c2 cells. In H9c2 cells, PF treatment reduced the formation of reactive oxygen species (ROS) induced by H/R. In H/R-stimulated H9c2 cells, PF also increased the activity of antioxidant enzymes such as superoxide dismutase and glutathione peroxidase. Furthermore, PF protected H9c2 cells against H/R-induced apoptosis, as demonstrated by increased Bcl-2 expression, decreased Bax expression, and decreased caspase-3 activity. Furthermore, PF increased the levels of p-AMPK and nuclear Nrf2 expression in response to H/R stimulation. AMPK inhibition, on the other hand, abolished the PF-mediated increase in Nrf2 signaling and the cardiac-protective effect in H9c2 cells exposed to H/R. These data suggest that PF protected H9c2 cells against H/R-induced oxidative stress and apoptosis through modulating the AMPK/Nrf2 signaling pathway. Our findings support the therapeutic potential of PF in myocardial I/R damage.

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Section: Introductionmentioning

confidence: 99%

Paeoniflorin Protects H9c2 Cardiomyocytes against Hypoxia/Reoxygenation Induced Injury via Regulating the AMPK/Nrf2 Signaling Pathway

Sun

Tan

et al. 2022

Evidence-Based Complementary and Alternative Medicine

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“…Similarly, a previous study reported that EA at Zusanli acupoint (ST36) can induce protective effects on myocardial injury in a rat model of sepsis by reducing myocardial NO level (Zhang et al, 2018). Other researchers found that EA pretreatment at Neiguan (PC6) acupoint can alleviate myocardial ischemia–reperfusion injury in rats with lower iNOS levels in the serum (Han et al, 2021). Another study suggested that EA at PC6 acupoint could prevent Doxorubicin‐induced cardiotoxicity through reducing NO production by decreasing the expression of iNOS in myocardial tissue of a mouse model (Wang et al, 2021).…”

Section: Discussionmentioning

confidence: 99%

Electroacupuncture at BL15 attenuates chronic fatigue syndrome by downregulating iNOS/NO signaling in C57BL/6 mice

Zhu

Wang

Yao

et al. 2022

The Anatomical Record

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Chronic fatigue syndrome (CFS) has a high incidence due to the increased pressure of daily life and work in modern society. Our previous clinical studies have found the effects of electroacupuncture (EA) on CFS patients, however, the mechanism of EA on CFS is still unknown. In this study, we investigated the effects of EA on cardiac function in a CFS mouse model to explore its underlying mechanism. The mice were randomly divided into three groups: control, CFS, and CFS mice receiving EA (CFS + EA). After behavioral assessments and echocardiographic measurement, blood and heart tissue of the mice were collected for biochemical tests, and then we evaluated the effects of EA on the CFS mouse model when nitric oxide (NO) levels were enhanced by l‐arginine. The results showed that EA ameliorated the injured motor and cardiac function. Meanwhile, EA also inhibited increased expression of inducible nitric oxide synthase (iNOS) at heart tissue and the serum NO levels in mice subjected to sustained forced swimming stress. Furthermore, the NO level in serum increased with l‐arginine administration, which blocked the effects of EA on CFS mice. This study suggested that EA could improve the motor function and cardiac function in CFS mice and its effects may be associated with the down‐regulation of iNOS/NO signaling.

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“…MIRI is common in patients with cardiovascular disease and in patients undergoing cardiopulmonary bypass and heart surgery [31]. Currently, pretreatment is often used in the treatment of MIRI and involves short-term non-destructive stimulation before injury onset in order to improve the tolerance of tissues or organs to subsequent permanent and fatal injury, and is considered one of the most effective mechanisms of endogenous protection [32]. EA pretreatment can attenuate MIRI and improve the quality of life of patients [13][14][15][16].…”

Section: Discussionmentioning

confidence: 99%

Mechanisms of Electroacupuncture Pretreatment in Alleviating Myocardial Ischemia Reperfusion Injury: Interactions between the Cerebellar Fastigial Nucleus and Lateral Hypothalamic Area

Zhang

et al. 2021

J Acupunct Meridian Stud

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Background: Myocardial ischemia reperfusion injury (MIRI) is an important mechanism of post-myocardial infarction injury and a main cause of death in patients with ischemic heart disease. Electroacupuncture (EA) pretreatment is effective for the prevention and treatment of MIRI, but mechanisms mediating the effects of cardiovascular disease EA treatments remain unclear. Objectives: To determine whether the lateral hypothalamus (LHA) and the cerebellar fastigial nucleus (FN) are involved in the protective effects of EA stimulation on MIRI. Methods: EA pretreatment was performed for 7 days before the establishment of the MIRI model. ST-segment changes on electrocardiograms were recorded and the Curtis-Walker arrhythmia score was used to evaluate changes in reperfusion injury. Hematoxylin-eosin staining was applied to evaluate the pathological and morphological changes in myocardial tissue. c-fos expression in the LHA and FN was determined by immunofluorescence staining. Glutamic (Glu) and γ-Aminobutyric acid (GABA) levels were measured using a high-performance liquid chromatography-electrochemical method. Results: EA pretreatment reduced ST-segment elevation, arrhythmia scores, and morphological changes in MIRI myocardial cells in rats, and decreased the c-fos protein expression in LHA/FN nuclei. MIRI was associated with an imbalance between GABA and Glu levels, whereas EA pretreatment increased GABA levels and decreased Glu levels in the LHA/FN. Conclusion: FN and LHA are involved in the EA-mediated attenuation of MIRI. Pretreatment with EA plays a protective role in the myocardium by regulating Glu and GABA release in the LHA and FN.

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Electroacupuncture Pretreatment Regulates Apoptosis of Myocardial Ischemia-Reperfusion Injury in Rats Through RhoA/p38MAPK Pathway Mediated by miR-133a-5p

Cited by 8 publications

References 27 publications

Paeoniflorin Protects H9c2 Cardiomyocytes against Hypoxia/Reoxygenation Induced Injury via Regulating the AMPK/Nrf2 Signaling Pathway

Paeoniflorin Protects H9c2 Cardiomyocytes against Hypoxia/Reoxygenation Induced Injury via Regulating the AMPK/Nrf2 Signaling Pathway

Electroacupuncture at BL15 attenuates chronic fatigue syndrome by downregulating iNOS/NO signaling in C57BL/6 mice

Mechanisms of Electroacupuncture Pretreatment in Alleviating Myocardial Ischemia Reperfusion Injury: Interactions between the Cerebellar Fastigial Nucleus and Lateral Hypothalamic Area

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