INHIBITORY EFFECTS OF MINOCYCLINE FOR PHOTORECEPTOR APOPTOSIS AFTER PHOTIC INJURY IN VIVO
碩士 === 國防醫學院 === 生理學研究所 === 90 === Photoreceptor degeneration is a multifactorial pathologic process. The pathogenetic mechanisms of many forms of photoreceptor degeneration are not definitively known, for example, in retinitis pigmentosa, retinal detachment, photic injury, age-related ma...
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ndltd-TW-090NDMC01160082015-10-13T10:16:50Z http://ndltd.ncl.edu.tw/handle/35469252424255098535 INHIBITORY EFFECTS OF MINOCYCLINE FOR PHOTORECEPTOR APOPTOSIS AFTER PHOTIC INJURY IN VIVO Minocycline對光傷害後造成感光細胞凋亡的抑制作用 Shing-Ting Hong 洪旭霆 碩士 國防醫學院 生理學研究所 90 Photoreceptor degeneration is a multifactorial pathologic process. The pathogenetic mechanisms of many forms of photoreceptor degeneration are not definitively known, for example, in retinitis pigmentosa, retinal detachment, photic injury, age-related macular degeneration, ischemic injury and other causes. Recent studies demonstrated that retinal photoreceptor cell died by apoptosis in both inherited and photic injury of retinal degeneration. In this experiment we evaluated the therapeutic efficacy of minocyline in photic injury of Lewis albino rats. Six to eight weeks old Lewis albino rats were reared for 2 weeks in cyclic light and dark adaptation for 24 hr before light exposure. The animals were divided into photic-injury and minocycline-treatment groups. The photic-injury groups were exposed to continuous light for 1 to 24 hours in 800-900 lux of light intensity. A dose of 100mg/kg-body weight of minocycline was injected intraperitoneally in minocycline-treatment groups. Light-exposed rats were killed after 24 hr of dark recovery following light exposure. Retinal damage after light exposure was evaluated by Western blot and the terminal transferase-mediated biotin dUTP nick end labeling (TUNEL) technique for identification of nicked/cleaved nuclear DNA. In photic-injury and minocycline-treatment groups, Western blot analysis showed the Caspase-3 active fragment from neural retina after 1,6,12,and 24 hours of light exposure. The degeneration of photoreceptor cells and retina pigment epithelium(RPE) worsened with the increasing duration of light exposure in histopathological study. The numbers of TUNEL positive nuclei were increase with the increasing duration of light exposure. Our findings confirmed earlier morphologic observations that photic exposure triggered apoptosis of photoreceptor cells. We believe that minocycline has partial inhibitory effects to photoreceptor apoptosis after photic injury. Keywords:photic injury、apoptosis、Caspase-3、TUNEL-stain、Western blot Jin-Nan Wu Cheng-Jong Chang 吳劍男 張正忠 2002 學位論文 ; thesis 72 zh-TW |
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碩士 === 國防醫學院 === 生理學研究所 === 90 === Photoreceptor degeneration is a multifactorial pathologic process. The pathogenetic mechanisms of many forms of photoreceptor degeneration are not definitively known, for example, in retinitis pigmentosa, retinal detachment, photic injury, age-related macular degeneration, ischemic injury and other causes. Recent studies demonstrated that retinal photoreceptor cell died by apoptosis in both inherited and photic injury of retinal degeneration. In this experiment we evaluated the therapeutic efficacy of minocyline in photic injury of Lewis albino rats. Six to eight weeks old Lewis albino rats were reared for 2 weeks in cyclic light and dark adaptation for 24 hr before light exposure. The animals were divided into photic-injury and minocycline-treatment groups. The photic-injury groups were exposed to continuous light for 1 to 24 hours in 800-900 lux of light intensity. A dose of 100mg/kg-body weight of minocycline was injected intraperitoneally in minocycline-treatment groups. Light-exposed rats were killed after 24 hr of dark recovery following light exposure. Retinal damage after light exposure was evaluated by Western blot and the terminal transferase-mediated biotin dUTP nick end labeling (TUNEL) technique for identification of nicked/cleaved nuclear DNA. In photic-injury and minocycline-treatment groups, Western blot analysis showed the Caspase-3 active fragment from neural retina after 1,6,12,and 24 hours of light exposure. The degeneration of photoreceptor cells and retina pigment epithelium(RPE) worsened with the increasing duration of light exposure in histopathological study. The numbers of TUNEL positive nuclei were increase with the increasing duration of light exposure. Our findings confirmed earlier morphologic observations that photic exposure triggered apoptosis of photoreceptor cells. We believe that minocycline has partial inhibitory effects to photoreceptor apoptosis after photic injury.
Keywords:photic injury、apoptosis、Caspase-3、TUNEL-stain、Western blot
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author2 |
Jin-Nan Wu |
author_facet |
Jin-Nan Wu Shing-Ting Hong 洪旭霆 |
author |
Shing-Ting Hong 洪旭霆 |
spellingShingle |
Shing-Ting Hong 洪旭霆 INHIBITORY EFFECTS OF MINOCYCLINE FOR PHOTORECEPTOR APOPTOSIS AFTER PHOTIC INJURY IN VIVO |
author_sort |
Shing-Ting Hong |
title |
INHIBITORY EFFECTS OF MINOCYCLINE FOR PHOTORECEPTOR APOPTOSIS AFTER PHOTIC INJURY IN VIVO |
title_short |
INHIBITORY EFFECTS OF MINOCYCLINE FOR PHOTORECEPTOR APOPTOSIS AFTER PHOTIC INJURY IN VIVO |
title_full |
INHIBITORY EFFECTS OF MINOCYCLINE FOR PHOTORECEPTOR APOPTOSIS AFTER PHOTIC INJURY IN VIVO |
title_fullStr |
INHIBITORY EFFECTS OF MINOCYCLINE FOR PHOTORECEPTOR APOPTOSIS AFTER PHOTIC INJURY IN VIVO |
title_full_unstemmed |
INHIBITORY EFFECTS OF MINOCYCLINE FOR PHOTORECEPTOR APOPTOSIS AFTER PHOTIC INJURY IN VIVO |
title_sort |
inhibitory effects of minocycline for photoreceptor apoptosis after photic injury in vivo |
publishDate |
2002 |
url |
http://ndltd.ncl.edu.tw/handle/35469252424255098535 |
work_keys_str_mv |
AT shingtinghong inhibitoryeffectsofminocyclineforphotoreceptorapoptosisafterphoticinjuryinvivo AT hóngxùtíng inhibitoryeffectsofminocyclineforphotoreceptorapoptosisafterphoticinjuryinvivo AT shingtinghong minocyclineduìguāngshānghàihòuzàochénggǎnguāngxìbāodiāowángdeyìzhìzuòyòng AT hóngxùtíng minocyclineduìguāngshānghàihòuzàochénggǎnguāngxìbāodiāowángdeyìzhìzuòyòng |
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