Effects of Acute Lithium Treatment on Brain Levels of Inflammatory Mediators in Poststroke Rats.

Matthew Boyko,Ahmad Nassar,Abed N Azab,Jacob Kaplanski,Yael Sharon-Granit,Alexander Zlotnik

doi:10.1155/2015/916234

Matthew Boyko, Ahmad Nassar + Show 4 more

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https://doi.org/10.1155/2015/916234

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Abstract

Stroke is a leading cause of mortality and morbidity worldwide. Few therapeutic options with proven efficacy are available for the treatment of this disabling disease. Lithium is the gold standard treatment for bipolar disorder. Moreover, lithium has been shown to exhibit neuroprotective effects and therapeutic efficacy as a treatment of other neurological disorders. This study was undertaken to examine the effects of lithium on brain inflammatory mediators levels, fever, and mortality in postischemic stroke rats. Ischemic stroke was induced by occlusion of the mid cerebral artery (MCAO). Pretreatment with a single dose of lithium at 2 hours before MCAO induction significantly reduced the elevation in interleukin- (IL-) 6 and prostaglandin E2 levels in brain of post-MCAO rats, as compared to vehicle-treated animals. On the other hand, lithium did not affect the elevation in IL-1α, IL-10, IL-12, and tumor necrosis factor-α levels in brain of post-MCAO rats. Moreover, pretreatment with lithium did not alter post-MCAO fever and mortality. These results suggest that acute pretreatment with a single dose of lithium did not markedly affect post-MCAO morbidity and mortality in rats.

Highlights

In 2004 the World Health Organization reported that stroke was the second cause of death worldwide after ischemic heart disease [1]
These results indicate that acute pretreatment with lithium did not significantly (P = 0.532) reduce the rate of poststroke mortality
The present study demonstrated that acute pretreatment with lithium did not prominently alter brain inflammation in post-mid cerebral artery occlusion (MCAO) rats

Summary

Introduction

In 2004 the World Health Organization reported that stroke was the second cause of death worldwide after ischemic heart disease [1]. Cerebrovascular disease was ranked as the first or second leading cause of burden of disease in the Western Pacific and European regions, respectively [1]. Those data clearly indicate that stroke is a very fatal and disabling disease. Postischemic inflammation involves activation of glial cells which produce cytotoxic and cytoprotective mediators [4]. After the occurrence of the ischemic injury, activated glial cells produce and secrete inflammatory mediators such as interleukin- (IL-) 1α, IL-1β, IL-6, IL-10, IL-12, nitric oxide, prostaglandin E2 (PGE2), and tumor necrosis factor- (TNF-) α [4,5,6,7]. Despite the data suggesting that poststroke inflammation harms infarct zone tissue, it is worth

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