June 2013
Volume 54, Issue 15
ARVO Annual Meeting Abstract  |   June 2013
Protective Effects of Chitosan on Ischemia-Reperfusion Injury in Rat Retina
Author Affiliations & Notes
  • Sheng-Li Cho
    National Taiwan University College of Medicine, Taipei, Taiwan
  • Chang-Hao Yang
    Department of Ophthalmology, National Taiwan University Hospital, Taipei, Taiwan
  • Footnotes
    Commercial Relationships Sheng-Li Cho, None; Chang-Hao Yang, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science June 2013, Vol.54, 6350. doi:
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      Sheng-Li Cho, Chang-Hao Yang; Protective Effects of Chitosan on Ischemia-Reperfusion Injury in Rat Retina. Invest. Ophthalmol. Vis. Sci. 2013;54(15):6350.

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

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Purpose: Nuclear factor-κB (NF-κB) is a key transcriptional factor in the regulation of oxidative stress and inflammatory mediators that are involved in tissue ischemia-reperfusion (IR) injury. Previous studies have shown that chitosan has anti-oxidative and anti-inflammatory properties. In this study, we investigated the expression of NF-κB in retina in a rat model of IR injury and evaluated the effect of chitosan on retina with IR injury.

Methods: Retinal ischemia was induced by increasing intraocular pressure to 130 mm Hg with normal saline infusion into anterior chamber in Wistar rats. Rats were treated with chitosan (10, and 20 mg/kg ip) 30 minutes before ischemia injury. At 24 hours and 7 days after the ischemia, retinal damage was evaluated. Dark-adapted full-field electroretinography (ERG) was performed to evaluate the functional change of retina. RT-PCR and western blotting were used to detect the expression of NF-κB and NF-κB related inflammatory genes expression. Immunohistochemistry were used to measure changes in the levels of cytokines and reactive oxygen species (ROS). Electrophoretic mobility shift assay (EMSA) was performed to evaluate the effect of chitosan on NF-κB activation in the retina of rats.

Results: Pretreatment with chitosan dose dependently inhibited the damage of the retina caused by IR injury. On the 7th postoperative day, the amplitudes of the ERG b-waves were significantly higher in the treatment group than in the control group. Chitosan suppressed the expression of NF-κB in the ischemia retina and the production of cytokines and ROS. EMSA demonstrated chitosan inhibited NF-κB activation in the retina of rats wit IR injury.

Conclusions: Chitosan attenuates retinal damage in IR injury by blocking NF-κB activation and NF-κB associated inflammatory cytokines production. Therefore, chitosan may provide a novel therapeutic strategy for the treatment of retinal ischemia reperfusion injury.

Keywords: 568 intraocular pressure • 688 retina • 572 ischemia  

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