June 2015
Volume 56, Issue 7
Free
ARVO Annual Meeting Abstract  |   June 2015
Neuroprotective effects of maltol on experimental glaucoma models
Author Affiliations & Notes
  • Samin Hong
    Ophthalmology, Yonsei University, Seoul, Korea (the Republic of)
  • Yookyung Song
    Ophthalmology, Yonsei University, Seoul, Korea (the Republic of)
  • Gong Je Seong
    Ophthalmology, Yonsei University, Seoul, Korea (the Republic of)
  • Footnotes
    Commercial Relationships Samin Hong, None; Yookyung Song, None; Gong Je Seong, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science June 2015, Vol.56, 2424. doi:
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      Samin Hong, Yookyung Song, Gong Je Seong; Neuroprotective effects of maltol on experimental glaucoma models. Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):2424.

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

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Abstract

Purpose: To investigate the neuroprotective effects of maltol, a natural aroma compound, on experimental glaucoma models.

Methods: For the in vitro study, mouse primary retinal ganglion cells (mRGCs) were isolated using immunopanning-magnetic separation and exposed to hydrogen peroxide (H2O2) in the presence of maltol. For the in vivo study, a total of 45 adult male C57BL/6 mice were used. The left optic nerve of each mouse was crushed for 10 seconds using self-closing forceps. 100 mg/kg of maltol was intraperitoneally injected for 5 consecutive days before (pre-treatment group, n=15) and after (post-treatment group, n=15) the crush injury. The RGC viability and apoptosis were determined by adenosine 5′-triphosphate (ATP) assay and terminal deoxynucleotidyl transferase (TdT)-mediated deoxyuridine triphosphate (dUTP) nick end labeling (TUNEL), respectively. The neurite outgrowth was assessed by immunofluorescence for α-tubulin. The activation of nuclear factor-κB (NF-κB) and mitogen-activated protein kinases (MAPKs; JNK, ERK, and p38) was also evaluated using immunofluorescence.

Results: When the primary mRGCs were exposed to 20 μM of H2O2 for 16 hours, their viability dropped to 40.3±3.4%. However, the maltol restored the cells in a dose-dependent manner. The viability recovered to 73.9±5.1% with 10 μM of maltol and even reached 175.1±11.3% with 2 mM of maltol, as measured by ATP assay. For both the in vitro and in vivo models, the glaucomatous injuries radically increased the number of TUNEL-positive mRGCs, but the maltol significantly reduced the proportion of those apoptotic cells. The active phosphorylated form of NF-κB and MAPKs was increased by the injuries but the maltol reduced it to an unstressful level.

Conclusions: Our data revealed that maltol attenuated the glaucomatous injuries in vitro and in vivo. Its neuroprotective effects seemed to be related to NF-κB and MAPKs signaling. Maltol has a potentiality to be used as a new neuroprotective therapeutic agent for glaucoma.

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