July 2018
Volume 59, Issue 9
Open Access
ARVO Annual Meeting Abstract  |   July 2018
Akebia Saponin D prevents axonal loss against TNF-induced optic nerve damage with autophagy modulation
Author Affiliations & Notes
  • Kana Sase
    Ophthalmology, St. Marianna University School of Medicine, Kawasaki, Kanagawa, Japan
  • Yasushi Kitaoka
    Ophthalmology, St. Marianna University School of Medicine, Kawasaki, Kanagawa, Japan
    Molecular Neuroscience, St. Marianna University Graduate School of Medicine, Kawasaki, Japan
  • Chihiro Tsukahara
    Ophthalmology, St. Marianna University School of Medicine, Kawasaki, Kanagawa, Japan
    Molecular Neuroscience, St. Marianna University Graduate School of Medicine, Kawasaki, Japan
  • Hitoshi Takagi
    Ophthalmology, St. Marianna University School of Medicine, Kawasaki, Kanagawa, Japan
  • Footnotes
    Commercial Relationships   Kana Sase, None; Yasushi Kitaoka, None; Chihiro Tsukahara, None; Hitoshi Takagi, None
  • Footnotes
    Support  KAKENHI 15K10908
Investigative Ophthalmology & Visual Science July 2018, Vol.59, 624. doi:
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      Kana Sase, Yasushi Kitaoka, Chihiro Tsukahara, Hitoshi Takagi; Akebia Saponin D prevents axonal loss against TNF-induced optic nerve damage with autophagy modulation
      . Invest. Ophthalmol. Vis. Sci. 2018;59(9):624.

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

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Abstract

Purpose : Akebia Saponin D (ASD), a triterpenoid saponin, has been shown to have neuroprotective effects in certain neuronal cells. The purpose of present study is to investigate whether ASD modulates tumor necrosis factor (TNF)-induced axonal loss and whether ASD alters autophagy machinery in optic nerves.

Methods : Rats were given intravitreal injection of TNF, concomitant injection of 2, 20, or 200 pmol ASD and TNF, or ASD alone. Immunoblot analysis was performed to examine p62 expression which is a marker of autophagic flux, in optic nerves 1 week after intravitreal injection. Morphometric analysis of axons was performed to evaluate the effects of ASD against TNF-induced optic nerve damage 2 weeks after intravitreal injection.

Results : p62 was increased significantly in the optic nerve after TNF injection, but this increase was totally inhibited by ASD. The ASD alone injection significantly declined p62 protein levels compared with the PBS-treated control level. Morphometric analysis showed robust axonal protective effects of ASD against TNF-induced optic nerve damage.

Conclusions : Decreased p62 expression by ASD may be associated with enhanced autophagic flux and this may be at least partly involved in its axonal protection.

This is an abstract that was submitted for the 2018 ARVO Annual Meeting, held in Honolulu, Hawaii, April 29 - May 3, 2018.

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