Anti-Inflammatory Effects of Melatonin in Obesity and Hypertension

Prado, Natalia Jorgelina; Ferder, León; Manucha, Walter; Diez, Emiliano

doi:10.1007/s11906-018-0842-6

Cited by 69 publications

(56 citation statements)

References 178 publications

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“…ob/ob mice showed, together with elevated blood pressure, a higher heart weight and cardiac hypertrophic index with respect to the control lean mice, but notably, melatonin supplementation significantly attenuated these obesity-related alterations. Our observations agree with previous studies in human and animal models in which melatonin reduced blood pressure to normal ranges (Agil et al, 2011;Prado et al, 2018). In the present study, we also observed that BNP heart expression is significantly lower in ob/ob mice compared to lean mice.…”

Section: Discussionsupporting

confidence: 94%

RETRACTED: Sirtuin1 Role in the Melatonin Protective Effects Against Obesity-Related Heart Injury

et al. 2020

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Integrative Physiology, a section of the journal Frontiers in PhysiologyObesity is a worldwide epidemic disease that induces important structural and functional changes to the heart and predisposes a patient to devastating cardiac complications. Sirtuin1 (SIRT1) has been found to have roles in regulating cardiac function, but whether it can help in cardioprotection is not clear. The aim of the present study was to determine whether melatonin, by modulating SIRT1 and in turn mitochondria signaling, may alleviate obesity-induced cardiac injuries. We investigated 10 lean control mice and 10 leptin-deficient obese mice (ob/ob) orally supplemented with melatonin for 8 weeks, as well as equal numbers of age-matched lean and ob/ob mice that did not receive melatonin. Hearts were evaluated using multiple parameters, including biometric values, morphology, SIRT1 activity and expression of markers of mitochondria biogenesis, oxidative stress, and inflammation. We observed that ob/ob mice experienced significant heart hypertrophy, infiltration by inflammatory cells, reduced SIRT1 activity, altered mitochondrial signaling and oxidative balance, and overexpression of inflammatory markers. Notably, melatonin supplementation in ob/ob mice reverted these obesogenic heart alterations. Melatonin prevented heart remodeling caused by obesity through SIRT1 activation, which, together with mitochondrial pathways, reduced oxidative stress and inflammation.Homogenized heart tissues were adequately processed for the quantitative measurement of natriuretic peptides type-B (BNP) protein level using a specific ELISA Kit (Novus Biologicals, Abingdon, United Kingdom), according to the manufacturer's Frontiers in Physiology | www.frontiersin.org

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Section: Discussionsupporting

confidence: 94%

RETRACTED: Sirtuin1 Role in the Melatonin Protective Effects Against Obesity-Related Heart Injury

et al. 2020

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“…Conduction disturbances in SCGx hearts could be related to the redistribution of connexin 43, and the lateralization of unphosphorylated forms of the Cx43 reported here and concurred with previous studies [23]. Our results are also relevant for other diseases with increased arrhythmic risk and chronodisruption like coronary artery disease, non-dipping hypertension, sleep apnea, obesity, and chronic kidney disease [5,10,16]. Especially, connexin 43 lateralization can aggravate pathologies with diminished conduction velocity due to fibrosis or genetic mutations [37,39,50].…”

Section: Discussionsupporting

confidence: 92%

Reperfusion Arrhythmias Increase after Superior Cervical Ganglionectomy Due to Conduction Disorders and Changes in Repolarization

Prado

Muñoz

Altamirano

et al. 2020

IJMS

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Pharmacological concentrations of melatonin reduce reperfusion arrhythmias, but less is known about the antiarrhythmic protection of the physiological circadian rhythm of melatonin. Bilateral surgical removal of the superior cervical ganglia irreversibly suppresses melatonin rhythmicity. This study aimed to analyze the cardiac electrophysiological effects of the loss of melatonin circadian oscillation and the role played by myocardial melatonin membrane receptors, SERCA2A, TNFα, nitrotyrosine, TGFβ, KATP channels, and connexin 43. Three weeks after bilateral removal of the superior cervical ganglia or sham surgery, the hearts were isolated and submitted to ten minutes of regional ischemia followed by ten minutes of reperfusion. Arrhythmias, mainly ventricular tachycardia, increased during reperfusion in the ganglionectomy group. These hearts also suffered an epicardial electrical activation delay that increased during ischemia, action potential alternants, triggered activity, and dispersion of action potential duration. Hearts from ganglionectomized rats showed a reduction of the cardioprotective MT2 receptors, the MT1 receptors, and SERCA2A. Markers of nitroxidative stress (nitrotyrosine), inflammation (TNFα), and fibrosis (TGFβ and vimentin) did not change between groups. Connexin 43 lateralization and the pore-forming subunit (Kir6.1) of KATP channels increased in the experimental group. We conclude that the loss of the circadian rhythm of melatonin predisposes the heart to suffer cardiac arrhythmias, mainly ventricular tachycardia, due to conduction disorders and changes in repolarization.

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“…Melatonin can also protect against the oxidative stress by improving the mitochondrial function, stimulating the expressions and activating the antioxidant enzymes including CAT, SOD, and GPx. 32 It is indicated that the potent anti-oxidative effect of melatonin is partially related to its lipophilic and hydrophilic properties, allowing it to easily transfer through all bio-barriers where it is highly available in subcellular organelles such as cell membrane and mitochondria. Regarding that the mitochondria is considered as the main site of ROS production, melatonin can strongly protect these organelles against the oxidative damage.…”

Section: Discussionmentioning

confidence: 99%

<p>Antioxidant and Anti-Inflammatory Properties of Melatonin in Patients with Type 2 Diabetes Mellitus with Periodontal Disease Under Non-Surgical Periodontal Therapy: A Double-Blind, Placebo-Controlled Trial</p>

Javid¹,

Hosseini²,

Gholinezhad³

et al. 2020

DMSO

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Background and Aim: The imbalance between pro-oxidant and antioxidant systems often leads to further oxidative damage in the pathogenesis of both diabetes and periodontal disease. This study aimed to investigate the antioxidant and anti-inflammatory properties of melatonin in type 2 diabetes mellitus (T2DM) patients with periodontal disease (PD) under non-surgical periodontal therapy (NSPT). Materials and Methods: In this double-blind clinical trial study, 50 T2DM patients with PD were randomly allocated to intervention and control groups and received 250 mg/day (2 tablets) either melatonin or placebo 1 h before bedtime for 8 weeks. The NSPT was performed for all patients in both groups at the beginning of the study. The serum levels of interleukin-1b (IL-1b), malondialdehyde (MDA), total antioxidant capacity (TAC), superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) were measured pre-and post-intervention. Results: Supplementation with melatonin in adjunct to NSPT significantly increased the serum levels of TAC, SOD, CAT, and GPx in the intervention group (P = 0.02, 0.008, 0.004 and 0.004, respectively). The mean changes of SOD, CAT, and GPx were significantly (P = 0.02, 0.04 and 0.04, respectively) greater in the intervention group compared with the control group. Also, after adjusting for confounding factors, the results did not change in terms of significance (P < 0.05). After the intervention, serum levels of MDA and IL-1b were significantly reduced in the intervention group (P < 0.001 and P = 0.008, respectively). The intervention group exhibited lower mean changes of MDA compared with the control group, and these changes were statistically significant (P = 0.008). In addition, after adjusting for confounding factors, the results did not change in terms of significance. Conclusion: The adjunctive effects of melatonin and NSPT may improve inflammatory and antioxidant parameters in T2DM patients with PD.

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Anti-Inflammatory Effects of Melatonin in Obesity and Hypertension

Cited by 69 publications

References 178 publications

RETRACTED: Sirtuin1 Role in the Melatonin Protective Effects Against Obesity-Related Heart Injury

RETRACTED: Sirtuin1 Role in the Melatonin Protective Effects Against Obesity-Related Heart Injury

Reperfusion Arrhythmias Increase after Superior Cervical Ganglionectomy Due to Conduction Disorders and Changes in Repolarization

<p>Antioxidant and Anti-Inflammatory Properties of Melatonin in Patients with Type 2 Diabetes Mellitus with Periodontal Disease Under Non-Surgical Periodontal Therapy: A Double-Blind, Placebo-Controlled Trial</p>

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