Neuroprotective and neurite outgrowth effects of maltol on retinal ganglion cells under oxidative stress

Samin Hong, Yoko Iizuka, Taekjune Lee, chanyun kim, Gong Je Seong

Research output: Contribution to journalArticle

18 Citations (Scopus)

Abstract

Purpose: To evaluate the neuroprotective and neurite outgrowth effects of maltol, a natural aroma compound, on retinal ganglion cells (RGCs) under oxidative stress in vitro.

Methods: Mouse primary RGCs were isolated using immunopanning–magnetic separation and exposed to H2O2 in the presence of maltol. The cell viability and apoptosis were determined by using adenosine 5′-t riphosphate (ATP) assay and terminal deoxynucleotidyl transferase (TdT)-mediated deoxyuridine triphosphate (dUTP) nick end labeling (TUNEL), respectively. Neurite outgrowth was assessed by immunofuorescence for α-tubulin. The activation of nuclear factor-κB (NF-κB) was also evaluated using immunofuorescence.

Results: When the RGCs were exposed to 20 μM of H2O2 for 16 h, their viability dropped to 40.3±3.4%. However, the maltol treatment 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. This oxidative stress signifcantly increased the number of TUNEL-positive RGCs, but the maltol drastically reduced the proportion of those apoptotic cells. The oxidative stress hampered the neurite outgrowth of the RGCs, whereas maltol restored their ability to sprout neurites. Regarding NF-κB, the active form of phosphorylated NF-κB (pNF-κB) increased the oxidative stress level but the maltol treatment again reduced it to an unstressful level.

Conclusions: Our data revealed that maltol attenuated the oxidative stress–induced injury in the primary mouse RGCs. Its neuroprotective and neurite outgrowth effects seemed to be related to NF-κB signaling. Maltol has potential as a new neuroprotective therapeutic agent for oxidative stress–related ocular diseases, including glaucoma.

Original languageEnglish
Pages (from-to)1456-1462
Number of pages7
JournalMolecular Vision
Volume20
Publication statusPublished - 2014 Oct 17

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Retinal Ganglion Cells
Oxidative Stress
Adenosine
maltol
Neuronal Outgrowth
DNA Nucleotidylexotransferase
Eye Diseases
Neuroprotective Agents
Neurites
Tubulin
Glaucoma
Cell Survival
Apoptosis

All Science Journal Classification (ASJC) codes

  • Ophthalmology

Cite this

Hong, Samin ; Iizuka, Yoko ; Lee, Taekjune ; kim, chanyun ; Seong, Gong Je. / Neuroprotective and neurite outgrowth effects of maltol on retinal ganglion cells under oxidative stress. In: Molecular Vision. 2014 ; Vol. 20. pp. 1456-1462.
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abstract = "Purpose: To evaluate the neuroprotective and neurite outgrowth effects of maltol, a natural aroma compound, on retinal ganglion cells (RGCs) under oxidative stress in vitro.Methods: Mouse primary RGCs were isolated using immunopanning–magnetic separation and exposed to H2O2 in the presence of maltol. The cell viability and apoptosis were determined by using adenosine 5′-t riphosphate (ATP) assay and terminal deoxynucleotidyl transferase (TdT)-mediated deoxyuridine triphosphate (dUTP) nick end labeling (TUNEL), respectively. Neurite outgrowth was assessed by immunofuorescence for α-tubulin. The activation of nuclear factor-κB (NF-κB) was also evaluated using immunofuorescence.Results: When the RGCs were exposed to 20 μM of H2O2 for 16 h, their viability dropped to 40.3±3.4{\%}. However, the maltol treatment 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. This oxidative stress signifcantly increased the number of TUNEL-positive RGCs, but the maltol drastically reduced the proportion of those apoptotic cells. The oxidative stress hampered the neurite outgrowth of the RGCs, whereas maltol restored their ability to sprout neurites. Regarding NF-κB, the active form of phosphorylated NF-κB (pNF-κB) increased the oxidative stress level but the maltol treatment again reduced it to an unstressful level.Conclusions: Our data revealed that maltol attenuated the oxidative stress–induced injury in the primary mouse RGCs. Its neuroprotective and neurite outgrowth effects seemed to be related to NF-κB signaling. Maltol has potential as a new neuroprotective therapeutic agent for oxidative stress–related ocular diseases, including glaucoma.",
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Neuroprotective and neurite outgrowth effects of maltol on retinal ganglion cells under oxidative stress. / Hong, Samin; Iizuka, Yoko; Lee, Taekjune; kim, chanyun; Seong, Gong Je.

In: Molecular Vision, Vol. 20, 17.10.2014, p. 1456-1462.

Research output: Contribution to journalArticle

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T1 - Neuroprotective and neurite outgrowth effects of maltol on retinal ganglion cells under oxidative stress

AU - Hong, Samin

AU - Iizuka, Yoko

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N2 - Purpose: To evaluate the neuroprotective and neurite outgrowth effects of maltol, a natural aroma compound, on retinal ganglion cells (RGCs) under oxidative stress in vitro.Methods: Mouse primary RGCs were isolated using immunopanning–magnetic separation and exposed to H2O2 in the presence of maltol. The cell viability and apoptosis were determined by using adenosine 5′-t riphosphate (ATP) assay and terminal deoxynucleotidyl transferase (TdT)-mediated deoxyuridine triphosphate (dUTP) nick end labeling (TUNEL), respectively. Neurite outgrowth was assessed by immunofuorescence for α-tubulin. The activation of nuclear factor-κB (NF-κB) was also evaluated using immunofuorescence.Results: When the RGCs were exposed to 20 μM of H2O2 for 16 h, their viability dropped to 40.3±3.4%. However, the maltol treatment 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. This oxidative stress signifcantly increased the number of TUNEL-positive RGCs, but the maltol drastically reduced the proportion of those apoptotic cells. The oxidative stress hampered the neurite outgrowth of the RGCs, whereas maltol restored their ability to sprout neurites. Regarding NF-κB, the active form of phosphorylated NF-κB (pNF-κB) increased the oxidative stress level but the maltol treatment again reduced it to an unstressful level.Conclusions: Our data revealed that maltol attenuated the oxidative stress–induced injury in the primary mouse RGCs. Its neuroprotective and neurite outgrowth effects seemed to be related to NF-κB signaling. Maltol has potential as a new neuroprotective therapeutic agent for oxidative stress–related ocular diseases, including glaucoma.

AB - Purpose: To evaluate the neuroprotective and neurite outgrowth effects of maltol, a natural aroma compound, on retinal ganglion cells (RGCs) under oxidative stress in vitro.Methods: Mouse primary RGCs were isolated using immunopanning–magnetic separation and exposed to H2O2 in the presence of maltol. The cell viability and apoptosis were determined by using adenosine 5′-t riphosphate (ATP) assay and terminal deoxynucleotidyl transferase (TdT)-mediated deoxyuridine triphosphate (dUTP) nick end labeling (TUNEL), respectively. Neurite outgrowth was assessed by immunofuorescence for α-tubulin. The activation of nuclear factor-κB (NF-κB) was also evaluated using immunofuorescence.Results: When the RGCs were exposed to 20 μM of H2O2 for 16 h, their viability dropped to 40.3±3.4%. However, the maltol treatment 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. This oxidative stress signifcantly increased the number of TUNEL-positive RGCs, but the maltol drastically reduced the proportion of those apoptotic cells. The oxidative stress hampered the neurite outgrowth of the RGCs, whereas maltol restored their ability to sprout neurites. Regarding NF-κB, the active form of phosphorylated NF-κB (pNF-κB) increased the oxidative stress level but the maltol treatment again reduced it to an unstressful level.Conclusions: Our data revealed that maltol attenuated the oxidative stress–induced injury in the primary mouse RGCs. Its neuroprotective and neurite outgrowth effects seemed to be related to NF-κB signaling. Maltol has potential as a new neuroprotective therapeutic agent for oxidative stress–related ocular diseases, including glaucoma.

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