April 2010
Volume 51, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2010
Retinal Protection From Ischemia-Reperfusion Injury Through Pharmacological Induction of Heme Oxygenase-1 by Cobalt Protoporphyrin
Author Affiliations & Notes
  • M.-H. Sun
    Ophthalmology, Chang Gung Memorial Hospital-Linkuo, Kwei-Shan, Taiwan
  • J.-H. Su Pang
    Graduate Institute of Clincal Medical Science, Chang Gung University, Kwei-Shan, Taiwan
  • K.-J. Chen
    Ophthalmology, Chang Gung Memorial Hospital-Linkuo, Kwei-Shan, Taiwan
  • L.-Y. Kao
    Ophthalmology, Chang Gung Memorial Hospital-Linkuo, Kwei-Shan, Taiwan
  • K.-K. Lin
    Ophthalmology, Chang Gung Memorial Hospital-Linkuo, Kwei-Shan, Taiwan
  • Y.-P. Tsao
    Ophthalmology, Mackay Memorial Hospital, Taipei, Taiwan
  • Footnotes
    Commercial Relationships  M.-H. Sun, None; J.-H. Su Pang, None; K.-J. Chen, None; L.-Y. Kao, None; K.-K. Lin, None; Y.-P. Tsao, None.
  • Footnotes
    Support  CMRPG370701E
Investigative Ophthalmology & Visual Science April 2010, Vol.51, 4700. doi:
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      M.-H. Sun, J.-H. Su Pang, K.-J. Chen, L.-Y. Kao, K.-K. Lin, Y.-P. Tsao; Retinal Protection From Ischemia-Reperfusion Injury Through Pharmacological Induction of Heme Oxygenase-1 by Cobalt Protoporphyrin. Invest. Ophthalmol. Vis. Sci. 2010;51(13):4700.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose: : To investigate the protective effects of cobalt protoporphyrin (CoPP), a potent heme oxygenase-1 (HO-1) inducer, in a rat model of ischemia-reperfusion injury, and to document the possible anti-apoptotic mechanisms underlying the protection in ischemia-reperfusion injury.

Methods: : Rats pretreated with intraperitoneal injection of CoPP 2 days before ischemia insult were subjected to retinal ischemia induced by increasing intraocular pressure to 130 mmHg for 60 minutes followed by 6 hours, 12 hours, 24 hours, and 7 days of reperfusion.

Results: : Pharmacological induction of HO-1 by CoPP led to HO-1 expression in retina. HO-1 overexpression alleviated the apoptosis in retina at 24 hours of reperfusion, preserved retinal ganglion cells and attenuated reduction of inner retina thickness 7 days after ischemia-reperfusion injury.

Conclusions: : Overexpression of HO-1 by pharmacological induction protected retina from subsequent cellular damage caused by ischemia-reperfusion injury through anti-apoptotic and anti-inflammatory effects.

Keywords: ischemia • apoptosis/cell death • inflammation 
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