Abstract
Both melatonin and electroacupuncture (EA) have been suggested to be effective treatments against stroke. However, it is unknown whether a combination of these two therapies could be beneficial against transient focal cerebral ischemia. The present study investigated the effects of pretreatment of a combination of melatonin and EA in a rat model of transient middle cerebral artery occlusion (MCAO). After pretreatment of melatonin plus EA (MEA), transient MCAO was induced for 90 minutes in male Sprague-Dawley (SD) rats. The neurological deficit score, brain infarct volume, cerebral edema ratio, neuronal inflammation, and apoptosis were evaluated 24 hours after transient MCAO. The expression of related inflammatory and apoptotic mediators in the brain was also investigated. The results showed that MEA improved neurological outcome, reduced brain infarct volume, and inhibited neuronal inflammation as well as apoptosis 24 hours after transient MCAO. The beneficial effects may derive from downregulation of proinflammatory and proapoptotic mediators and upregulation of antiapoptotic mediators. Thus, these results suggest a preventive effect of pretreatment of MEA on transient focal cerebral ischemia.
Highlights
Stroke is a serious cerebral vascular event with increasing prevalence worldwide especially in the society with aging of the population, and ischemic stroke is the most common type
No significant difference was observed between the control and melatonin plus EA (MEA) groups at the same time points during ischemia and reperfusion (P > 0.05), as shown in Tables 2, 3, and 4
Increasing evidence shows that pretreatment with various kinds of neuroprotectants induces beneficial effects against stroke in animal models; many of them have limitations and adverse effects that may prevent the clinical application in patients [33, 34]
Summary
Stroke is a serious cerebral vascular event with increasing prevalence worldwide especially in the society with aging of the population, and ischemic stroke is the most common type. Many neuroprotectants have been investigated; they were effective in animals but not in stroke patients [2,3,4]. Owing to the narrow therapeutic time window [5, 6] and a substantial risk of hemorrhagic complications, clinical use of rtPA is limited to a small number of stroke patients [7]. Broader attention to integrated therapeutics has been advocated repeatedly for treating ischemic stroke to increase the chance of success [4, 8, 9]. Accumulating lines of evidence have demonstrated the efficacy of pretreatment therapies which could induce neuroprotection against cerebral ischemic injury
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