Abstract
The present review paper supports the approach to deliver melatonin and to target melatonin receptors for neuroprotection in stroke. We discuss laboratory evidence demonstrating neuroprotective effects of exogenous melatonin treatment and transplantation of melatonin-secreting cells in stroke. In addition, we describe a novel mechanism of action underlying the therapeutic benefits of stem cell therapy in stroke, implicating the role of melatonin receptors. As we envision the clinical entry of melatonin-based therapeutics, we discuss translational experiments that warrant consideration to reveal an optimal melatonin treatment strategy that is safe and effective for human application.
Highlights
Melatonin is a hormone produced in the pineal gland, which has long been established as primary modulator of circadian rhythms in mammals [1,2,3,4]
We have demonstrated that chronic exogenous treatment with melatonin protects against experimental stroke [52]
While there are studies which reported therapeutic outcomes following exogenous melatonin treatment [143,144,158], our study provides a complementary approach of combining melatonin and Amniotic epithelial cells (AEC) for achieving more effective neuroprotection [53,54]
Summary
Melatonin is a hormone produced in the pineal gland, which has long been established as primary modulator of circadian rhythms in mammals [1,2,3,4]. Many antioxidants have been tested in experimental stroke models and have reached clinical trials (Tables 1 and 2) In comparison with these substances, melatonin has an obvious advantage because it is an endogenous substance. Melatonin administration after experimental stroke reduces infarction volume [41,42] Such a protective effect is seen in both gray and white matter [43]. Melatonin secretion is known to decrease age dependently [48], suggesting that if melatonin directly affects stroke aged people should suffer more strongly from insults of stroke This may be ameliorated with melatonin pretreatment; studies in animal models of stroke have demonstrated that pretreatment of melatonin exerts anti-inflammatory effects and reduces infarction volume [49,50,51]. Thereafter, we discuss key translational research needed to facilitate clinical trials of melatonin treatment and transplantation of melatonin-secreting cells
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