Minocycline improves cardiac function after myocardial infarction in rats by inhibiting activation of PARP-1

Zhao, Hua; Zhang, Jianjun; Hong, Gang

doi:10.1016/j.biopha.2017.10.053

Cited by 8 publications

(4 citation statements)

References 24 publications

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“…Reactive oxygen species produced during oxidative stress damage membrane lipids, proteins, DNA thereby causing apoptosis of cardiomyocytes and eventually resulting in cardiac dysfunction [26]. Infiltration of inflammatory cells in the myocardium after an ischemic event initiates an exaggerated inflammatory response, this further accelerates and worsens ventricular remodeling by increasing myocardial injury [27]. Higher levels of the inflammatory marker TNF-α have been associated with ventricular dilation and cardiac fibrosis.…”

Section: Discussionmentioning

confidence: 99%

Ginseng Berry Extract Rich in Phenolic Compounds Attenuates Oxidative Stress but not Cardiac Remodeling post Myocardial Infarction

Parikh

Raj

et al. 2019

IJMS

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The cardioprotective effects of ginseng root extracts have been reported. However, nothing is known about the myocardial actions of the phenolic compounds enriched in ginseng berry. Therefore, this study was undertaken to investigate the effects of American ginseng berry extract (GBE) in an experimental model of myocardial infarction (MI). Coronary artery ligation was performed on Sprague–Dawley male rats to induce MI after which animals were randomized into groups receiving either distilled water or GBE intragastrically for 8 weeks. Echocardiography and assays for malondialdehyde (MDA) and TNF-α were conducted. Flow cytometry was used to test the effects of GBE on T cell phenotypes and cytokine production. Although GBE did not improve the cardiac functional parameters, it significantly attenuated oxidative stress in post-MI rat hearts. GBE treatment also resulted in lower than control levels of TNF-α in post-MI rat hearts indicating a strong neutralizing effect of GBE on this cytokine. However, there was no effect of GBE on the proportion of different T cell subsets or ex-vivo cytokine production. Taken together, the present study demonstrates GBE reduces oxidative stress, however no effect on cardiac structure and function in post-MI rats. Moreover, reduction of TNF-α levels below baseline raises concern regarding its use as prophylactic or preventive adjunct therapy in cardiovascular disease.

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Section: Discussionmentioning

confidence: 99%

Ginseng Berry Extract Rich in Phenolic Compounds Attenuates Oxidative Stress but not Cardiac Remodeling post Myocardial Infarction

Parikh

Raj

et al. 2019

IJMS

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show abstract

“…Namely, minocycline induced upregulation of MCPIP1 and reduction of NF-κB activation and pro-in ammatory mediator secretion. Another study showed, beside downregulation of NF-κB and pro-in ammatory factor expression, improvement of cardiac contractility and prevention of cardiac remodeling after experimental myocardial infarction [29]. It was shown that minocycline could decrease poly-(ADP-ribose) polymerase-1 (PARP-1) expression and activation, thus alleviating the cardiac dysregulation.…”

Section: Discussionmentioning

confidence: 99%

Antioxidative and Cardioprotective Effects of Minocycline in Ischemia/reperfusion Injury in Experimental Model of Hypertension

Rudic,

Stojanovic,

Sobot

et al. 2024

Preprint

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Purpose: Cardiovascular diseases remains leading cause of death and disabilities. Coronary artery occlusion and consequent ischemia leads to acute myocardial infarction, but restoration of blood flow provokes further myocardial damage known as reperfusion injury. Minocycline is possessing anti-inflammatory and anti-apoptotic activity, immune-modulating and antioxidative properties besides its primary antibacterial effect. Recently it gained significant interest in preventing cardiac damage especially due to myocardial ischemia/reperfusion injury (MI/RI). The aim of this study was to assess protective ability of preconditioning and postconditioning of isolated hearts from healthy and spontaneously hypertensive rats with minocycline, on functional recovery and redox status after MI/RI using Langendorfftechnique. Methods: Using sensor in left ventricle, the cardiodynamic parameters were recorded and in the samples of the coronary venous effluent oxidative stress biomarkers were analyzed. Minocycline was injected directly into the coronary vessels, in preconditioning 5 min before global ischemia, and in postconditioning during the first 5 min of reperfusion. Results: Changes in redox balance induced by minocycline were more pronounced in postconditioning fashion of application. Cardioprotective effects of minocycline due to MI/RI are even more pronounced in hypertensive hearts. Conclusion: Minocycline showed significant cardioprotective effects, which was more pronounced in hypertensive compared to healthy hearts. Reduction of pro-oxidative biomarkers was more pronounced in hypertensive hearts compared to the normotensive, especially if it is applied in the form of post-conditioning. The fact that better effects are achieved during postconditioning is particularly important, bearing in mind that it is not possible to predict the occurrence of a heart attack.

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“…Indeed, galectin-3 was markedly up-regulated in the myocardium and cardiomyocyte in response to ischemia/reperfusion and hypoxia/reoxygenation, respectively ( Zhang et al, 2020 ; Redondo et al, 2021 ). Ischemia/hypoxia is well-known to cause cardiomyocyte death by activating caspase-3 and subsequent cleavage of PARP-1 protein ( Zhao et al, 2018 ; Li et al, 2020b ). Thus, COX2, galectin-3, and cleaved PARP-1 are often determined as the index for inflammatory response, apoptosis and fibrosis.…”

Section: Discussionmentioning

confidence: 99%

Upregulation of Small Ubiquitin-Like Modifier 2 and Protein SUMOylation as a Cardioprotective Mechanism Against Myocardial Ischemia-Reperfusion Injury

Zhao

Zhang

et al. 2021

Front. Pharmacol.

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Background: Small ubiquitin-like modifier (SUMO) proteins modify proteins through SUMOylation as an essential protein post-translational modification (PTM) for regulating redox status, inflammation, and cardiac fibrosis in myocardial infarction. This study aimed to investigate whether natural product puerarin could alleviate myocardial ischemia/reperfusion injury (MI-RI) by targeting protein SUMOylation.Methods: Mouse MI-RI model was induced by ligating the left anterior descending (LAD) coronary artery and subsequently treated with puerarin at the dose of 100 mg/kg. Rat cardiomyocyte H9c2 cells were challenged by hypoxia/reoxygenation and treated with puerarin at concentrations of 10, 20, and 40 μM. The infarction area of mouse hearts was assessed by 2% TTC staining. Cell damage was analyzed for the release of lactate dehydrogenase (LDH) in serum and cell culture medium. Western blot technique was employed to detect the expression of SUMO2, phospho-ERK, pro-inflammatory biomarker COX2, fibrosis index galectin-3, apoptosis-related protein cleaved PARP-1. The activation of the estrogen receptor (ER) pathway was assayed by the dual-luciferase reporter system.Results: The present study validated that puerarin effectively reduced myocardial infarct size and LDH release in the mouse MI-RI model. In the cell culture system, puerarin effectively decreased the release of LDH and the protein level of COX2, galectin-3, and cleaved PARP-1. Mechanistic studies revealed that puerarin increased the expression of SUMO2, SUMOylation of proteins and the activation of ER/ERK pathway in cardiomyocytes. ER, ERK and SUMO2 inhibitors attenuated the cardioprotective effects of puerarin.Conclusion: Puerarin may alleviate myocardial injury by promoting protein SUMOylation through ER/ERK/SUMO2-dependent mechanism.

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Minocycline improves cardiac function after myocardial infarction in rats by inhibiting activation of PARP-1

Cited by 8 publications

References 24 publications

Ginseng Berry Extract Rich in Phenolic Compounds Attenuates Oxidative Stress but not Cardiac Remodeling post Myocardial Infarction

Ginseng Berry Extract Rich in Phenolic Compounds Attenuates Oxidative Stress but not Cardiac Remodeling post Myocardial Infarction

Antioxidative and Cardioprotective Effects of Minocycline in Ischemia/reperfusion Injury in Experimental Model of Hypertension

Upregulation of Small Ubiquitin-Like Modifier 2 and Protein SUMOylation as a Cardioprotective Mechanism Against Myocardial Ischemia-Reperfusion Injury

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