June 2013
Volume 54, Issue 15
Free
ARVO Annual Meeting Abstract  |   June 2013
Protective effects of an PPAR-γ agonist on retinal ischemia/reperfusion injury in rats
Author Affiliations & Notes
  • Xiaoyan Zhang
    Ophthalmology, Huashan Hospital affiliated to Shanghai Fudan University, Shanghai, China
  • Yi-qin Xiao
    Ophthalmology, Huashan Hospital affiliated to Shanghai Fudan University, Shanghai, China
  • Yu Zhang
    Ophthalmology, Huashan Hospital affiliated to Shanghai Fudan University, Shanghai, China
  • Jiaying zhang
    Ophthalmology, Huashan Hospital affiliated to Shanghai Fudan University, Shanghai, China
  • Wen Ye
    Ophthalmology, Huashan Hospital affiliated to Shanghai Fudan University, Shanghai, China
  • Footnotes
    Commercial Relationships Xiaoyan Zhang, None; Yi-qin Xiao, None; Yu Zhang, None; Jiaying zhang, None; Wen Ye, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science June 2013, Vol.54, 6316. doi:
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      Xiaoyan Zhang, Yi-qin Xiao, Yu Zhang, Jiaying zhang, Wen Ye; Protective effects of an PPAR-γ agonist on retinal ischemia/reperfusion injury in rats. Invest. Ophthalmol. Vis. Sci. 2013;54(15):6316.

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

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Abstract
 
Purpose
 

To investigate the protective effects of an PPAR-γ agonist in the rat retina after ischemia/reperfusion (I/R) injury.

 
Methods
 

Retinal ischemia was induced in rats by increasing the intraocular pressure to 110mmHg for 60 minutes. The PPAR-γ agonist was delivered by periocular injection and intraperitoneal injection before I/R. Seven days after I/R injury, retinal damage was quantified by measuring the thickness of the retina, the functional changes of VEP and ERG, and the RGC number. The expression of GFAP, NF-κB p65 in the retina was determined by western blot, real-time polymerase chain reaction (PCR), and immunohistochemistry.

 
Results
 

I/R caused severe disruption of the retinal construction and integrity. In I/R group without treatment the number of RGCs was reduced by 53%. The PPAR-γ agonist either delivered by periocular injection or by intraperitoneal injection preserved the thickness of the retina after I/R, and the survival of RGC was 77% and 74% respectively. Pretreated with the PPAR-γ agonist also attenuate the destruction of VEP and ERG caused by I/R. The amplitudes of the ERG b-waves and the VEP P1-N2 component were significantly lower in the I/R group than in the groups pretreated with the PPAR-γ agonist (p<0.01). After ischemia, expression of GFAP, NF-κB p65 subunit was upregulated and high phosphoration level of p65 subunit was detected in retina. The PPAR-γ agonist pretreatment suppressed NF-κB activation and reduced the GFAP overexpression.

 
Conclusions
 

The PPAR-γ agonist promotes the survival of RGCs and protect retina histological integrity as well as retinal function after retinal I/R. The protect effect appears to act through the anti-inflammatory effects towards the inhibition of retinal glia activation, suggesting that the PPAR-γ agonist may have a therapeutic potential for the prevention of retinal diseases associated with I/R.

 
 
Hematoxylin and eosin staining of retina . (A) shows the retina of I/R group.The PPAR-γ agonist pretreatment maintained the thickness of the whole retina, IPL and INL after I/R (B,C). (D) shows the retina tissue of the normal control group. ip., intraperitoneal injection; po., periocular injection.
 
Hematoxylin and eosin staining of retina . (A) shows the retina of I/R group.The PPAR-γ agonist pretreatment maintained the thickness of the whole retina, IPL and INL after I/R (B,C). (D) shows the retina tissue of the normal control group. ip., intraperitoneal injection; po., periocular injection.
 
 
Retrograde labeled RGCs in wholemount retinas 7 days after ocular ischemia. ip., intraperitoneal injection; po., periocular injection.
 
Retrograde labeled RGCs in wholemount retinas 7 days after ocular ischemia. ip., intraperitoneal injection; po., periocular injection.
 
Keywords: 572 ischemia • 688 retina • 656 protective mechanisms  
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