Low-dose carbon monoxide inhalation protects neuronal cells from apoptosis after optic nerve crush
作者： Zeli Chen , Ruobing Wang , Jiangchun Wu , Fangzhou Xia , Qinglei Sun
DOI: 10.1016/J.BBRC.2015.12.064
关键词:
摘要: Glaucomatous optic neuropathy, including axonal degeneration and apoptotic death of retinal ganglion cells (RGCs), eventually leads to irreversible visual impairment. Carbon monoxide (CO) acts as a therapeutic agent against neural injury via its anti-apoptotic effect. Here we hypothesized that low-dose CO inhalation can protect RGCs in rat model nerve crush (ONC). ONC was performed on adult male Sprague Dawley rats imitate glaucomatous damage. Low-dose (250 ppm) or air inhaled for 1 h immediately after ONC, all the tests were carried out 2 weeks later. Flash evoked potentials (FVEP) pupil light relax (PLR) recorded assessment function. RGC density evaluated by hematoxylin eosin staining Fluorogold labeling. Retinal process assessed TUNEL caspase-3 activity measurement. treatment significantly ameliorated abnormalities FVEP PLR induced ONC. As expected, increased remarkably insult. Moreover, decreased number TUNEL-positive cell layer attenuated activity. protects from inhibiting dependent apoptosis.
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