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Review
. 2023 Aug 4:15:1227513.
doi: 10.3389/fnagi.2023.1227513. eCollection 2023.

Melatonin: a promising neuroprotective agent for cerebral ischemia-reperfusion injury

Majid Tozihi  1 , Behrouz Shademan  2 , Hadi Yousefi  3 , Cigir Biray Avci  4 , Alireza Nourazarian  3 , Gholamreza Dehghan  1
Affiliations
Review

Melatonin: a promising neuroprotective agent for cerebral ischemia-reperfusion injury

Majid Tozihi et al. Front Aging Neurosci. .

Abstract

Cerebral ischemia-reperfusion (CIR) injury is initiated by the generation of reactive oxygen species (ROS), which leads to the oxidation of cellular proteins, DNA, and lipids as an initial event. The reperfusion process impairs critical cascades that support cell survival, including mitochondrial biogenesis and antioxidant enzyme activity. Failure to activate prosurvival signals may result in increased neuronal cell death and exacerbation of CIR damage. Melatonin, a hormone produced naturally in the body, has high concentrations in both the cerebrospinal fluid and the brain. However, melatonin production declines significantly with age, which may contribute to the development of age-related neurological disorders due to reduced levels. By activating various signaling pathways, melatonin can affect multiple aspects of human health due to its diverse range of activities. Therefore, understanding the underlying intracellular and molecular mechanisms is crucial before investigating the neuroprotective effects of melatonin in cerebral ischemia-reperfusion injury.

Keywords: cerebral ischemia-reperfusion injury; ischemic strokes; melatonin; neuroprotective agent; reactive oxygen species (ROS).

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

FIGURE 1
FIGURE 1
The mechanisms underlying the protective effects of melatonin on brain damage caused by cerebral-IRI. Cyt c, cytochrome c; SOD, superoxide dismutase; CAT, catalase; MDA, malonaldehyde; HO-1, heme oxygenase-1.
See this image and copyright information in PMC

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References

    1. Abolhasanpour N., Alihosseini S., Golipourkhalili S., Badalzadeh R., Mahmoudi J., Hosseini L. (2021). Effect of melatonin on endoplasmic reticulum-mitochondrial crosstalk in stroke. Arch. Med. Res. 52 673–682. 10.1016/j.arcmed.2021.04.002 - DOI - PubMed
    1. Ajoolabady A., Shademan B., Avci C. B., Nikanfar M., Nourazarian A., Laghousi D. (2022). Diagnostic potential of autophagy-5 protein, apolipoprotein B-48, and oxidative stress markers in serum of patients with early-stage ischemic stroke. World Neurosurg. 167 e656–e663. 10.1016/j.wneu.2022.08.063 - DOI - PubMed
    1. Alghamdi B. S. (2018). The neuroprotective role of melatonin in neurological disorders. J. Neurosci. Res. 96 1136–1149. 10.1002/jnr.24220 - DOI - PMC - PubMed
    1. Amanakis G., Kleinbongard P., Heusch G., Skyschally A. (2019). Attenuation of ST-segment elevation after ischemic conditioning maneuvers reflects cardioprotection online. Basic Res. Cardiol. 114:22. 10.1007/s00395-019-0732-3 - DOI - PubMed
    1. Andrabi S. S., Parvez S., Tabassum H. (2015). Melatonin and ischemic stroke: Mechanistic roles and action. Adv. Pharm. Sci. 2015:384750. 10.1155/2015/384750 - DOI - PMC - PubMed

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