March 2012
Volume 53, Issue 14
Free
ARVO Annual Meeting Abstract  |   March 2012
Neuroprotective Effects of Epigallocatechin-3-gallate against N-methyl-D-aspartate Induced Excitotoxicity in Rat Retina
Author Affiliations & Notes
  • Libin Jiang
    Eye Center, Beijing Tongren Hospital, Beijing, China
  • Fei Chen
    Eye Center, Beijing Tongren Hospital, Beijing, China
  • Ningli Wang
    Eye Center, Beijing Tongren Hospital, Beijing, China
  • Footnotes
    Commercial Relationships  Libin Jiang, None; Fei Chen, None; Ningli Wang, None
  • Footnotes
    Support  National Natural Science Foundation of China (No.30973268)
Investigative Ophthalmology & Visual Science March 2012, Vol.53, 6574. doi:
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      Libin Jiang, Fei Chen, Ningli Wang; Neuroprotective Effects of Epigallocatechin-3-gallate against N-methyl-D-aspartate Induced Excitotoxicity in Rat Retina. Invest. Ophthalmol. Vis. Sci. 2012;53(14):6574.

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

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Abstract

Purpose: : Epigallocatechin-3-gallate (EGCG), the major polyphenol of green tea, is an antioxidant exhibiting multifunctional properties, and has been reported to exhibit anti-inflammatory, anti-apoptosis, and neuroprotective effects. Since recent studies suggested that EGCG can also reduce glutamate excitotoxicity, we investigated the potentially protective effects of EGCG against NMDA (N-methyl-D-aspartate)-induced excitotoxicity in the retina.

Methods: : Female Wistar rats (n=171) were divided into a normal control group without any procedure performed (n=9); a saline control group undergoing an intravitreal saline injection (n=54); an NMDA control group receiving an intravitreal NMDA injection and intraperitoneal saline injections (n=54); and an NMDA study group (n=54) receiving an intravitreal NMDA injection plus intraperitoneal EGCG (25mg/kg) injections. Starting at two days prior to the intravitreal injection, the intraperitoneal injections were performed daily for the whole study period. At 12 hours, 1, 2, 3 days, 1 and 2 weeks after the intravitreal injection, the animals were sacrificed. Neurons in the retinal ganglion cell layer (GCL) on histological sections were counted, the thickness of Thy-1 immunoreactivity measured and the expression of Thy-1 mRNA by real-time-polymerase chain reaction assessed.

Results: : At all time points of follow-up, neural cell density in the GCL, thickness of Thy-1 immunoreactivity, and expression of Thy-1 mRNA were significantly (all P<0.05) lower in the NMDA control group than in the NMDA study group, in which the parameters were significantly (all P<0.05) lower than in the saline control group and the normal control group. In both groups with intravitreal NMDA injections, NMDA associated neural cell loss in the GCL, thickness of Thy-1 immunoreactivity and expression of Thy-1 mRNA decreased significantly with increasing follow-up time. Neural cell density in the GCL, thickness of Thy-1 immunoreactivity and expression of Thy-1 mRNA three parameters did not differ significantly (P>0.05) between the normal control group and the saline control group.

Conclusions: : Intraperitoneal application of EGCG resulted in a significantly less marked NMDA induced loss of retinal ganglion cells. It suggests a protective effect of the EGCG on retinal ganglion cell loss in this experimental NMDA model.

Keywords: neuroprotection • retina 
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