Inhibiting Cardiac Mitochondrial Fatty Acid Oxidation Attenuates Myocardial Injury in a Rat Model of Cardiac Arrest

Wang, Peng; Zhang, Fan; Pan, Liming; Tan, Yunke; Song, Fang; Ge, Qiulin; Huang, Zitong; Yao, Lan

doi:10.1155/2021/6622232

Cited by 4 publications

(3 citation statements)

References 30 publications

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“…Therefore, mitochondrial dysfunction is a characteristic of I/R injury. 5 Recently, ferroptosis, a newly discovered form of iron-dependent cell death, has attracted growing attention. Moreover, it has been reported that ferroptosis is involved in rat heart I/R injury, rather than ischemic injury.…”

Section: Introductionmentioning

confidence: 99%

Ferulic Acid Alleviates Myocardial Ischemia Reperfusion Injury Via Upregulating AMPKα2 Expression-Mediated Ferroptosis Depression

Liu

Gong

et al. 2021

Journal of Cardiovascular Pharmacology

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:Ferroptosis, a recently discovered form of regulated cell death that is characterized by iron accumulation and excessive reactive oxygen species generation, has been favored by most researchers. Increasing evidence suggest that ferulic acid (FA) could exert marked effects to myocardial ischemia reperfusion (I/R) injury, although the understanding of its molecular mechanism is still limited. In our study, the myocardial I/R injury model was established to explore the relationship between I/R injury and ferroptosis. First, we successfully constructed myocardial I/R injury model with changes in ST segment, increased creatine phosphokinase, lactate dehydrogenase activities, and N-Terminal Pro Brain Natriuretic Peptide content, and a significantly larger infarct size. Then, the increased levels of the Ptgs2 mRNA, Fe2+ accumulation, and a decreased reduced glutathione/oxidized glutathione disulfide ratio were detected in ischemia-reperfusion-injured heart, which is highly consistent with ferroptosis. However, these effects were significantly improved after FA treatment. Based on these results, FA increased the activities of the antioxidant enzymes superoxide dismutase, catalase and glutathione peroxidase, decreased the malondialdehyde level, ameliorated the production of reactive oxygen species, and promoted the generation of adenosine triphosphate. These effects of FA are similar to those of the ferroptosis inhibitor ferrostatin-1. Upregulation of AMPKα2 and Glutathione Peroxidase 4 expression were also observed in the FA group. Compound C, a specific Adenosine 5'-monophosphate (AMP)-activated protein kinase inhibitor, significantly blocked the protective effect of FA. These findings underlined that FA inhibits ferroptosis by upregulating the expression of AMPKα2 and serves as a cardioprotective strategy.

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Section: Introductionmentioning

confidence: 99%

Ferulic Acid Alleviates Myocardial Ischemia Reperfusion Injury Via Upregulating AMPKα2 Expression-Mediated Ferroptosis Depression

Liu

Gong

et al. 2021

Journal of Cardiovascular Pharmacology

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“…[ 77 ] Moreover, inhibiting myocardial mitochondrial FAO may protect the myocardium by reducing the production of reactive oxygen species. [ 78 ] Aldosterone has been reported to increase oxidative stress and promote inflammation and fibrosis of the heart. [ 79 ] A recent randomized controlled trial has found that spironolactone, an aldosterone antagonist, could relieve heart failure with preserved EF (HfpEF), reducing the markers of fibrosis in circulation.…”

Section: Treatment Strategies Of Cteph and Their Effects On The Rvmentioning

confidence: 99%

Right ventricle remodeling in chronic thromboembolic pulmonary hypertension

Liu

Yang

Tian

et al. 2022

Journal of Translational Internal Medicine

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Chronic thromboembolic pulmonary hypertension (CTEPH) is an underdiagnosed, but potentially curable pulmonary vascular disease. The increased pulmonary vascular resistance in CTEPH is caused by unresolved proximal thrombus and secondary microvasculopathy in the pulmonary vasculature, leading to adaptive and maladaptive remodeling of the right ventricle (RV), eventual right heart failure, and death. Knowledge on the RV remodeling process in CTEPH is limited. The progression to RV failure in CTEPH is a markedly slower process. A detailed understanding of the pathophysiology and underlying mechanisms of RV remodeling may facilitate early diagnosis and the development of targeted therapy. While ultrasound, magnetic resonance imaging, right heart catheterization, and serum biomarkers have been used to assess cardiac function, the current treatment strategies reduce the afterload of the right heart, but are less effective in improving the maladaptive remodeling of the right heart. This review systematically summarizes the current knowledge on adaptive and maladaptive remodeling of the right heart in CTEPH from molecular mechanisms to clinical practice.

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“…The animal preparation techniques used in this study have been previously reported (6,19). Briefly, rats were anesthetized with sodium pentobarbital (45 mg/kg).…”

Section: Cardiac Arrest Modelmentioning

confidence: 99%

Baicalein Relieves Brain Injury via Inhibiting Ferroptosis and Endoplasmic Reticulum Stress in a Rat Model of Cardiac Arrest

Zhou¹,

Zhang²,

Wang³

et al. 2022

Shock

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Background: Cardiac arrest (CA) is one of the leading causes of death worldwide. Endoplasmic reticulum (ER) stress and ferroptosis are proven pathological mechanisms implicated in neuronal damage. Baicalein, a ferroptosis Inhibitor, improved outcomes after traumatic brain injury. We aimed to explore the effects of baicalein on brain injury via ferroptosis and ER stress in a rat model of CA. Methods: Cardiac arrest models were established in Sprague-Dawley (SD) rats. The sham group (n = 6) was untreated with inducing ventricular fibrillation to cardiac arrest and cardiopulmonary resuscitation (CPR). Survival rats were randomly divided into five groups (n = 6). Ferroptosis inhibitor and ER stress agonist were administered separately and together in three groups. There was no drug intervention in the remaining group. The neurological deficit scores were recorded. Characteristics of ferroptosis were observed. And the associated protein of ferroptosis and ER stress were determined by Western blot. Cerebral ROS production was measured by using 2′,7′-dichlorofluorescein diacetate as the oxidative fluorescent probe. Results: Baicalein treatment improved neurological outcomes and decreased neurocyte injuries compared with CPR group. The changes of ferroptosis, more specifically, iron content, glutathione peroxidase 4 (GPX4), reactive oxygen species (ROS), arachidonate 15-lipoxygenase (ALOX15) and mitochondrial characteristics, were observed in brain tissue after ROSC. ALOX15 was lower in baicalein group than in CPR group. The morphology and structure of mitochondria in baicalein group were better than in CPR group. The ER stress markers, glucose-regulated protein 78, activating Transcription Factor 4 and C/EBP homologous protein was lower in baicalein group compared with CPR group. ROS in tunicamycin group was higher than in CPR group. And ROS in baicalein +tunicamycin group was lower than in tunicamycin group. Conclusion: Ferroptosis and ER stress are both involved in brain injury after ROSC. Baicalein alleviates brain injury via suppressing the ferroptosis and ER stress, and reduces ROS partly through inhibiting ER stress. Baicalein is a potential drug to relieve brain injury after ROSC.

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Inhibiting Cardiac Mitochondrial Fatty Acid Oxidation Attenuates Myocardial Injury in a Rat Model of Cardiac Arrest

Cited by 4 publications

References 30 publications

Ferulic Acid Alleviates Myocardial Ischemia Reperfusion Injury Via Upregulating AMPKα2 Expression-Mediated Ferroptosis Depression

Ferulic Acid Alleviates Myocardial Ischemia Reperfusion Injury Via Upregulating AMPKα2 Expression-Mediated Ferroptosis Depression

Right ventricle remodeling in chronic thromboembolic pulmonary hypertension

Baicalein Relieves Brain Injury via Inhibiting Ferroptosis and Endoplasmic Reticulum Stress in a Rat Model of Cardiac Arrest

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