ABSTRACT
Neurological disorders are often marked by oxidative stress, an increase in damage by free radicals (Du et al. 1996, Lee et al. 1999, Nakao et al. 1995). This correlation hints at the potential of free radical scavengers (e.g., deprenyl, 7-nitroindazole, iron chelator, vitamin E) for therapeutic treatments, especially considering the capability of free radical scavengers and antioxidants in preventing cell death (Leker et al. 2002, Suzuki et al. 2002). Due to the observed negative impact of oxidative stress on the pathophysiology and behavior of stroke victims, administration of free radical scavengers and antioxidants may serve as an effective treatment to lessen the detrimental effects of ischemic injury. In fact, numerous antioxidants have made it to clinical trials after extensive preclinical research. Melatonin, however, because of its endogenous nature, may prove even more effective than its antioxidative stress properties would suggest alone. The transplantation of melatonin-secreting cells, postischemic injury, has incredible potential as a melatonin-based therapy for stroke. Transplantation of melatonin-secreting pineal glands into rats as well as exogenous melatonin treatment have both been found to stimulate neuroprotection (Borlongan et al. 2000, 2003). Melatonin receptor type 1A (MT1) has been implicated in the neuroprotective mechanism of action for stem cells in in vivo stroke models (Kaneko et al. 2011).
