Low-dose XXXX inhalation protects neuronal cells from apoptosis after optic nerve crush.

@entity227 @entity1223 @entity16 @entity1711 @entity18489 @entity1781 @entity1710 @entity35 @entity4124 @entity528 @entity130
UNASSIGNED: @entity1781 , including @entity528 and apoptotic death of retinal ganglion cells (RGCs), eventually leads to irreversible @entity227 . @entity1223 (CO) acts as a therapeutic agent against @entity130 via its anti-apoptotic effect. Here we hypothesized that low-dose CO inhalation can protect RGCs in a @entity35 model of optic nerve crush (ONC). ONC was performed on adult male @entity35 to imitate glaucomatous @entity16 . Low-dose CO (250  ppm) or air was inhaled for 1  h immediately after ONC, and all the tests were carried out 2 weeks later. Flash visual evoked potentials (FVEP) and pupil light relax (PLR) were recorded for the assessment of visual function. RGC density was evaluated by @entity1710 and @entity1711 staining and Fluorogold labeling. Retinal apoptotic process was assessed by TUNEL staining and @entity4124 activity measurement. Low-dose CO treatment significantly ameliorated the abnormalities of FVEP and PLR induced by ONC. As expected, the RGC density was increased remarkably by CO inhalation after the glaucomatous @entity1781 . Moreover, CO treatment after ONC significantly decreased the number of TUNEL-positive cells in ganglion cell layer and attenuated the retinal @entity4124 activity. Low-dose CO inhalation protects RGCs from @entity18489 via inhibiting @entity4124 dependent apoptosis.
