Melatonin: Still a forgotten antioxidant

Abreu-González, Pedro

doi:10.1016/j.ijcard.2011.02.070

Cited by 12 publications

(12 citation statements)

References 12 publications

(23 reference statements)

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“…20 A large number of studies have demonstrated the powerful capability of melatonin and its metabolites, both at physiological and at pharmacological concentrations, to oppose oxidative damage by scavenging free radicals. [21][22][23][24][25] Furthermore, special emphasis has been given to the protective effect of melatonin against atherosclerosis progression, which involves the normalization of lipid profiles and improvements in endothelial function and anti-inflammatory effects. [26][27][28] Notably, some physiological effects of melatonin have been identified as mediated through melatonin receptors, including membrane type 1 (MT1) present in mammalian arteries.…”

Section: Introductionmentioning

confidence: 99%

Melatonin Attenuates Aortic Endothelial Permeability and Arteriosclerosis in Streptozotocin-Induced Diabetic Rats

Tang

Zhang

et al. 2015

J Cardiovasc Pharmacol Ther

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The development of diabetic macrovascular complications is a multifactorial process, and melatonin may possess cardiovascular protective properties. This study was designed to evaluate whether melatonin attenuates arteriosclerosis and endothelial permeability by suppressing the myosin light-chain kinase (MLCK)/myosin light-chain phosphorylation (p-MLC) system via the mitogen-activated protein kinase (MAPK) signaling pathway or by suppressing the myosin phosphatase-targeting subunit phosphorylation (p-MYPT)/p-MLC system in diabetes mellitus (DM). Rats were randomly divided into 4 groups, including control, high-fat diet, DM, and DM + melatonin groups. Melatonin was administered (10 mg/kg/d) by gavage for 12 weeks. The DM significantly increased the serum fasting blood glucose and lipid levels, as well as insulin resistance and endothelial dysfunction, which were attenuated by melatonin therapy to various extents. Importantly, the aortic endothelial permeability was significantly increased in DM rats but was dramatically reversed following treatment with melatonin. Our findings further indicated that hyperglycemia and hyperlipidemia enhanced the expressions of MLCK, p-MYPT, and p-MLC, which were partly associated with decreased membrane type 1 expression, increased extracellular signal-regulated kinase (ERK) phosphorylation, and increased p38 expression. However, these changes in protein expression were also significantly reversed by melatonin. Thus, our results are the first to demonstrate that the endothelial hyperpermeability induced by DM is associated with increased expressions of MLCK, p-MYPT, and p-MLC, which can be attenuated by melatonin at least partly through the ERK/p38 signaling pathway.

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Section: Introductionmentioning

confidence: 99%

Melatonin Attenuates Aortic Endothelial Permeability and Arteriosclerosis in Streptozotocin-Induced Diabetic Rats

Tang

Zhang

et al. 2015

J Cardiovasc Pharmacol Ther

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“…It has a wide range of reported biologic effects including antioxidative [21]–[26], anti-inflammatory and antitumor activities [27]–[34] and has generated considerable interest as a pharmaceutical compound with a wide range of therapeutic activities. Melatonin has also been shown to possess chemotherapeutic potential in human cancers and to be capable of modulating several signal transduction pathways associated with cell survival, proliferation, apoptosis and invasion [35]–[39].…”

Section: Introductionmentioning

confidence: 99%

Melatonin Inhibits the Migration of Human Lung Adenocarcinoma A549 Cell Lines Involving JNK/MAPK Pathway

et al. 2014

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ObjectiveMelatonin, an indolamine produced and secreted predominately by the pineal gland, exhibits a variety of physiological functions, possesses antioxidant and antitumor properties. But, the mechanisms for the anti-cancer effects are unknown. The present study explored the effects of melatonin on the migration of human lung adenocarcinoma A549 cells and its mechanism.MethodsMTT assay was employed to measure the viability of A549 cells treated with different concentrations of melatonin. The effect of melatonin on the migration of A549 cells was analyzed by wound healing assay. Occludin location was observed by immunofluorescence. The expression of occludin, osteopontin (OPN), myosin light chain kinase (MLCK) and phosphorylation of myosin light chain (MLC), JNK were detected by western blots.ResultsAfter A549 cells were treated with melatonin, the viability and migration of the cells were inhibited significantly. The relative migration rate of A549 cells treated with melatonin was only about 20% at 24 h. The expression level of OPN, MLCK and phosphorylation of MLC of A549 cells were reduced, while the expression of occludin was conversely elevated, and occludin located on the cell surface was obviously increased. The phosphorylation status of JNK in A549 cells was also reduced when cells were treated by melatonin.ConclusionsMelatonin significantly inhibits the migration of A549 cells, and this may be associated with the down-regulation of the expression of OPN, MLCK, phosphorylation of MLC, and up-regulation of the expression of occludin involving JNK/MAPK pathway.

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“…Indeed, PEDF not only inhibits retinal endothelial cell growth and migration, but also suppresses ischemia-induced retinal neovascularization [2,3]. Moreover, we have found that PEDF prevents vascular remodeling after balloon angioplasty and improves cardiac function in a rat model of acute myocardial infarction [4,5]. These observations suggest that PEDF may also exert beneficial effects on ischemic heart disease as well as atherosclerosis.…”

Section: To the Editormentioning

confidence: 76%

“…Thus, melatonin readily enters all cardiomyocytes and subcellular compartments with highest concentrations possibly being present in membranes, mitochondria and nuclei [3]. Recent data also suggest that the mechanism of protection of melatonin appears to involve, at least in part, the inhibition of mitochondrial permeability transition pore opening via prevention of cardiolipin peroxidation [4,5].…”

Section: To the Editormentioning

confidence: 99%

Melatonin and cardioprotection in the acute myocardial infarction: A promising cardioprotective agent

Abreu-González

Reíter

2012

International Journal of Cardiology

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Melatonin: Still a forgotten antioxidant

Cited by 12 publications

References 12 publications

Melatonin Attenuates Aortic Endothelial Permeability and Arteriosclerosis in Streptozotocin-Induced Diabetic Rats

Melatonin Attenuates Aortic Endothelial Permeability and Arteriosclerosis in Streptozotocin-Induced Diabetic Rats

Melatonin Inhibits the Migration of Human Lung Adenocarcinoma A549 Cell Lines Involving JNK/MAPK Pathway

Melatonin and cardioprotection in the acute myocardial infarction: A promising cardioprotective agent

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