Compound 49b Reduces Inflammatory Markers and Apoptosis after Ocular Blast Injury
Annual rept. 15 Aug 2013-14 Aug 2014
TENNESSEE UNIV CENTER FOR THE HEALTH SCIENCES MEMPHIS
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In year 2 of this project, we determined whether Compound 49b, a novel beta-adrenergic receptor agonist, prevented increased inflammatory and apoptosis proteins in insulin-like growth factor binding protein 3 IGFBP-3 knockout KO mice after exposure to ocular blast. Eyes from IGFBP-3 KO mice were exposed to a blast of air from a paintball gun at 26psi. Eyes were collected at 4, 24, and 72 hours after blast exposure. In a subset of mice, Compound 49b eye drops 1mM dose were applied within 4 hours, 24 hours, or 72 hours after blast. Three days after exposure to blast, all mice were sacrificed. One eye was used for protein analyses of TNF , IL-1 , Bax, Bcl-xL, caspase 3, and cytochrome C. We found that ocular exposure to 26psi of air pressure led to a significant increase in both inflammatory and apoptotic proteins. When Compound 49b was applied within 4 or 24 hours after blast, it mitigated the increase in inflammatory and apoptotic proteins. Ocular blast produces a significant increase in inflammatory and apoptotic proteins in the retina, specifically in retinal ganglion cells. These proteins are reduced after treatment with a topical beta-adrenergic receptor agonist. This data suggests local application of beta-adrenergic receptor agonists may be protective in ocular blast.
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