April 2011
Volume 52, Issue 14
ARVO Annual Meeting Abstract  |   April 2011
Lens Epithelial Cell Protection from Ultraviolet Radiation Using Grape Seed Extract
Author Affiliations & Notes
  • Heather L. Chandler
    Optometry, The Ohio State University, Columbus, Ohio
  • Carmen M. Colitz
    OcuGLO Rx & Aquatic Animal Eye Care, Jupiter, Florida
  • Footnotes
    Commercial Relationships  Heather L. Chandler, None; Carmen M. Colitz, OcuGLO Rx (I, E)
  • Footnotes
    Support  None
Investigative Ophthalmology & Visual Science April 2011, Vol.52, 1555. doi:
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    • Get Citation

      Heather L. Chandler, Carmen M. Colitz; Lens Epithelial Cell Protection from Ultraviolet Radiation Using Grape Seed Extract. Invest. Ophthalmol. Vis. Sci. 2011;52(14):1555.

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

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Purpose: : To determine the impact of grape seed extract (GSE) on canine lens epithelial cells (LEC) following exposure to ultraviolet (UV) radiation.

Methods: : Primary cultures of canine LEC (n=4) were pretreated with 0 or 50 µg/mL GSE prior to UV exposure (300 J/m2), and allowed to recover. In concurrent experiments, cultured LEC (n=4) were UV irradiated and allowed to recover the presence of GSE (doses ranging from 0 - 50 µg/mL). Cell viability in all treatment groups was assessed via MTT assay. To evaluate LEC apoptosis, a cytochrome c release assay and a caspase-3 activity assay were used. Immunoblot analysis was performed to evaluate the expression of phosphorylated JNK (pJNK) in LEC following UV and GSE treatments. Nonparametric statistical tests were used to compare outcomes accounting for treatment group and UV exposure status.

Results: : Both LEC pretreated with GSE prior to UV irradiation and LEC allowed to recover from UV exposure in the presence of GSE, demonstrated a significant increase in cell viability compared to controls (p<0.05). Following irradiation, apoptosis in LEC was increased; treatment with GSE significantly (p=0.002) reduced UV-induced LEC apoptosis. In addition, GSE was able to significantly (p=0.002) lower pJNK protein expression relative to irradiated control LEC, in which pJNK expression was increased.

Conclusions: : GSE was capable of reducing UV induced LEC apoptosis, potentially through the pJNK signaling pathway. In combination with previous data, there is evidence that GSE could potentially protect LEC from the damaging effects of UV and subsequent oxidative stress.

Keywords: antioxidants • apoptosis/cell death • oxidation/oxidative or free radical damage 

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