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Youde Jiang, Jena Steinle; Compound 49b protects against blast-induced retinal injury. Invest. Ophthalmol. Vis. Sci. 2013;54(15):1183.
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To determine whether Compound 49b, a novel beta-adrenergic receptor agonist, can prevent increased inflammatory and apoptotic markers in mice after exposure to ocular blast
Eyes from C57/BL6 mice were exposed to a blast of air from a paintball gun at 26psi. Eyes were collected 4 hours, 24 hours, and 72 hours after blast exposure. In a subset of mice, Compound 49b eye drops (1mM) were applied within 4 hours, 24 hours, or 72 hours of blast. Three days after exposure of blast, all mice were sacrificed. One eye was used for measurement of retinal proteins, TNFα, IL-1B, Bax, Bcl-xL, caspase 3 and cytochrome C. The other eye was used for TUNEL labeling of apoptotic cells.
We found that ocular exposure to 26psi air pressure led to a significant increase in apoptotic and inflammatory mediators within 4 hours and throughout the time period investigated. When Compound 49b was initiated within 4 hours or 24 hours of blast injury, levels of apoptotic and inflammatory mediators was significantly reduced. Application of Compound 49b within 72 hours of blast injury reduced inflammatory mediators but not to untreated levels.
Ocular blast injury produces a significant increase in key inflammatory and apoptotic markers in the retina as early as 4 hours after blast exposure. These inflammatory and apoptotic markers are significantly reduced if a beta-adrenergic receptor agonist is applied within 24 hours of blast exposure. Taken together, data suggest that local application of beta-adrenergic receptor agonists may be beneficial for the retina to reduce inflammatory and apoptotic markers.
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