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Masoud A. Fard, Neil R. Miller, Katayoon B. Ebrahimi, Steve L. Bernstein; The Effect Of Intravitreal Rock Inhibitor (H1152p) On Inflammation, RGC Loss And Axonal Regeneration In Experimental Model Of Adult Rodent Anterior Ischemic Optic Neuropathy. Invest. Ophthalmol. Vis. Sci. 2011;52(14):4670.
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© ARVO (1962-2015); The Authors (2016-present)
To analyze the outcomes of Rho-kinase (ROCK) inhibition on inflammation,retinal ganglion cell (RGC) survival and axonal regenerationin an experimental model of adult rodent anterior ischemic opticneuropathy.
Anterior ischemic optic neuropathy was induced with a novelphotoembolic mechanism. Immunohistochemistry and Western blotwere performed to detect activation of RhoA signaling and inflammation.Specific ROCK-inhibitor H-1152P was administered intravitreallyone day after ischemia The extent of inflammation, RGC lossand axonal regeneration was determined after 8 and 14 days.
After the ischemic event, we observed severe inflammation, RhoAactivity and RGC loss. RGC loss was significantly reduced inresponse to 1µM H-1152P. This was associated with a decreasein the level of inflammatory cells. H-1152P also resulted inaxonal regeneration after optic nerve ischemia.
These results demonstrate the neuroprotective effect of H-1152P-mediatedROCK-inhibition on retinal ganglion cells after ischemia.
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