Apigenin attenuates myocardial ischemia/reperfusion injury via the inactivation of p38 mitogen-activated protein kinase

Yang, Xia; Yang, Junlan; Hu, Jing; Li, Xiaoqing; Zhang, Xianjiao; Li, Fulin

doi:10.3892/mmr.2015.4293

Cited by 43 publications

(23 citation statements)

References 25 publications

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“…In a long-term study of diabetic cardiomyopathy in mice, apigenin administration improves left ventricular functions in the heart [ 40 ]. Apigenin also improves the recovery of cardiac function during ischemia/reperfusion injury of isolated rat heart using Langedorff system [ 23 ]. Thus, our data on apigenin-mediated recovery of myocardial injury and cardiac dysfunction may lead to potential therapeutic development in sepsis.…”

Section: Resultsmentioning

confidence: 99%

“…Cardioprotective effects of apigenin have been reported in numerous studies. Apigenin ameliorates myocardial ischemia/reperfusion injury via the inactivation of p38 mitogen-activated protein kinase [ 23 ]. Apigenin reduces the blood pressure, heart weight, heart weight index, cardiomyocyte cross-sectional area, and serum angiotensin II in a cardiac hypertrophy model via HIF-1 and PPAR α pathways [ 24 ].…”

Section: Introductionmentioning

confidence: 99%

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Apigenin Alleviates Endotoxin‐Induced Myocardial Toxicity by Modulating Inflammation, Oxidative Stress, and Autophagy

Lang

Zhang

et al. 2017

Oxidative Medicine and Cellular Longevity

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Apigenin, a component in daily diets, demonstrates antioxidant and anti-inflammatory properties. Here, we intended to explore the mechanism of apigenin-mediated endotoxin-induced myocardial injury and its role in the interplay among inflammation, oxidative stress, and autophagy. In our lipopolysaccharide- (LPS-) induced myocardial injury model, apigenin ameliorated cardiac injury (lactate dehydrogenase (LDH) and creatine kinase (CK)), cell death (TUNEL staining, DNA fragmentation, and PARP activity), and tissue damage (cardiac troponin I (cTnI) and cardiac myosin light chain-1 (cMLC1)) and improved cardiac function (ejection fraction (EF) and end diastolic left ventricular inner dimension (LVID)). Apigenin also alleviated endotoxin-induced myocardial injury by modulating oxidative stress (nitrotyrosine and protein carbonyl) and inflammatory cytokines (TNF-α, IL-1β, MIP-1α, and MIP-2) along with their master regulator NFκB. Apigenin modulated redox homeostasis, and its anti-inflammatory role might be associated with its ability to control autophagy. Autophagy (determined by LAMP1, ATG5, and p62), its transcriptional regulator transcription factor EB (TFEB), and downstream target genes including vacuolar protein sorting-associated protein 11 (Vps11) and microtubule-associated proteins 1A/1B light chain 3B (Map1lc3) were modulated by apigenin. Thus, our study demonstrated that apigenin may lead to potential development of new target in sepsis treatment or other myocardial oxidative and/or inflammation-induced injuries.

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Apigenin Alleviates Endotoxin‐Induced Myocardial Toxicity by Modulating Inflammation, Oxidative Stress, and Autophagy

Lang

Zhang

et al. 2017

Oxidative Medicine and Cellular Longevity

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“…Moreover, p38 inhibition with an antioxidant during ischemia–reperfusion is associated with improved cardiac recovery, decreased infarct size, and reduced apoptosis [ 66 ]. This was related to increased endogenous anti-oxidative enzyme activity and inhibition of oxidative stress [ 67 ]. The antioxidant Peroxiredoxin 1 and the ROS scavenger N-acetyl-l-cysteine have been also shown to decrease oxidative stress and block the activation of p38 and JNK, thus reducing apoptosis during ischemia–reperfusion [ 68 ].…”

Section: P38 In Ischemia–reperfusion Injurymentioning

confidence: 99%

p38 MAPK Pathway in the Heart: New Insights in Health and Disease

Romero-Becerra

Santamans

Folgueira

et al. 2020

IJMS

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The p38 mitogen-activated kinase (MAPK) family controls cell adaptation to stress stimuli. p38 function has been studied in depth in relation to cardiac development and function. The first isoform demonstrated to play an important role in cardiac development was p38α; however, all p38 family members are now known to collaborate in different aspects of cardiomyocyte differentiation and growth. p38 family members have been proposed to have protective and deleterious actions in the stressed myocardium, with the outcome of their action in part dependent on the model system under study and the identity of the activated p38 family member. Most studies to date have been performed with inhibitors that are not isoform-specific, and, consequently, knowledge remains very limited about how the different p38s control cardiac physiology and respond to cardiac stress. In this review, we summarize the current understanding of the role of the p38 pathway in cardiac physiology and discuss recent advances in the field.

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“…In murine and rat models baicalein (30 mg/kg), apigenin (5 mg/kg) and vitexin (6, 3, 1.5 mg/kg) reduced I/R injury-induced infarct size, apoptosis, pro-inflammatory cytokines and oxidative stress [162,163,164]. Employing diabetic rats subjected to myocardial I/R, it has been assessed the protective effects of luteolin or breviscapine, a flavonoid extracted by Erigeron breviscapus .…”

Section: In Vivo Effects Of Polyphenols Against Oxidative Stress-imentioning

confidence: 99%

Effects of Polyphenols on Oxidative Stress-Mediated Injury in Cardiomyocytes

et al. 2017

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Cardiovascular diseases are the main cause of mortality and morbidity in the world. Hypertension, ischemia/reperfusion, diabetes and anti-cancer drugs contribute to heart failure through oxidative and nitrosative stresses which cause cardiomyocytes nuclear and mitochondrial DNA damage, denaturation of intracellular proteins, lipid peroxidation and inflammation. Oxidative or nitrosative stress-mediated injury lead to cardiomyocytes apoptosis or necrosis. The reactive oxygen (ROS) and nitrogen species (RNS) concentration is dependent on their production and on the expression and activity of anti-oxidant enzymes. Polyphenols are a large group of natural compounds ubiquitously expressed in plants, and epidemiological studies have shown associations between a diet rich in polyphenols and the prevention of various ROS-mediated human diseases. Polyphenols reduce cardiomyocytes damage, necrosis, apoptosis, infarct size and improve cardiac function by decreasing oxidative stress-induced production of ROS or RNS. These effects are achieved by the ability of polyphenols to modulate the expression and activity of anti-oxidant enzymes and several signaling pathways involved in cells survival. This report reviews current knowledge on the potential anti-oxidative effects of polyphenols to control the cardiotoxicity induced by ROS and RNS stress.

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Apigenin attenuates myocardial ischemia/reperfusion injury via the inactivation of p38 mitogen-activated protein kinase

Cited by 43 publications

References 25 publications

Apigenin Alleviates Endotoxin‐Induced Myocardial Toxicity by Modulating Inflammation, Oxidative Stress, and Autophagy

Apigenin Alleviates Endotoxin‐Induced Myocardial Toxicity by Modulating Inflammation, Oxidative Stress, and Autophagy

p38 MAPK Pathway in the Heart: New Insights in Health and Disease

Effects of Polyphenols on Oxidative Stress-Mediated Injury in Cardiomyocytes

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