Melatonin improves nitric oxide bioavailability in isoproterenol induced myocardial injury
Isoproterenol administration is associated with cardiac inflammation and decreased NO availability. Melatonin has been reported to have cardioprotective effect. The aim of this study was to investigate the effect of melatonin on NO bioavailability and inflammation in myocardial injury induced by iso...
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Published in: | Molecular and cellular endocrinology Vol. 591; p. 112279 |
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Main Authors: | , , , , , , , , , , , , , |
Format: | Journal Article |
Language: | English |
Published: |
Ireland
Elsevier B.V
15-09-2024
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Subjects: | |
Online Access: | Get full text |
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Summary: | Isoproterenol administration is associated with cardiac inflammation and decreased NO availability. Melatonin has been reported to have cardioprotective effect. The aim of this study was to investigate the effect of melatonin on NO bioavailability and inflammation in myocardial injury induced by isoproterenol. Isoproterenol was administrated in male Wistar rats for 7 days to induce cardiac injury. The animals were divided into 3 groups: Control, Isoproterenol, Isoproterenol + Melatonin. Animals received melatonin for 7 days. Echocardiographic analysis was performed and the hearts were collected for molecular analysis. Animals that received isoproterenol demonstrated a reduction in left ventricle systolic and diastolic diameter, indicating the presence of concentric hypertrophy. Melatonin was able to attenuate this alteration. Melatonin also improved NO bioavailability and decreased NF-κβ, TNFα and IL-1β expression. In conclusion, melatonin exhibited a cardioprotective effect which was associated with improving NO bioavailability and decreasing the pro-inflammatory proteins.
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•Excess adrenergic activity causes inflammation and decreased NO availability.•Melatonin has been reported to have cardioprotective effect.•This study investigate the effect of melatonin in isoproterenol-induced heart injury.•Melatonin exhibited a cardioprotective effect.•Melatonin increased NO bioavailability and decreased pro-inflammatory markers. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0303-7207 1872-8057 1872-8057 |
DOI: | 10.1016/j.mce.2024.112279 |