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Short Communication: Agmatine inhibits hypoxia-induced TNF-α release from cultured retinal ganglion cells

SAMIN HONG, KYOUNGSOO PARK, CHAN YUN KIM, GONG JE SEONG
Institute of Vision Research, Department of Ophthalmology, Yonsei University College of Medicine, Seoul, Republic of Korea
Address correspondence to: Gong Je Seong, MD, PhD. Institute of Vision Research, Department of Ophthalmology, Yongdong Severance Hospital, Yonsei University College of Medicine, 14692 Dogok-dong, Kangnam-gu, Seoul 135-720, REPUBLIC OF KOREA. Fax: 82-2-3463-1049. E-mail: gjseong@yuhs.ac

BIOCELL 2008, 32(2), 201-205. https://doi.org/10.32604/biocell.2008.32.201

Abstract

The effect of hypoxia on the release of tumor necrosis factor-α (TNF-α) in transformed rat retinal ganglion cells (RGCs) and the effect of agmatine on the hypoxia-induced production of TNF-α in RGCs were evaluated. RGCs were cultured under hypoxic conditions with 5% oxygen, with or without 100 μM agmatine. The expression levels of TNF-α and its receptor-1 (TNF-R1) were investigated by Western blot analysis. After 6 hours of hypoxia, we noted an increase in TNF-α production in RGCs. Agmatine significantly reduced TNF-α level after 12 hours of hypoxic treatment. The expression of TNF-R1 was not affected by the hypoxia or agmatine treatment. Our results show that agmatine inhibits the TNF-α production of RGCs in hypoxic condition. These results demonstrate a possible neuroprotective mechanism for agmatine against hypoxic damage in RGCs.

Keywords

retinal ganglion cell, tumor necrosis factor-α, hypoxia, agmatine.

Cite This Article

HONG,, S. (2008). Short Communication: Agmatine inhibits hypoxia-induced TNF-α release from cultured retinal ganglion cells. BIOCELL, 32(2), 201–205.

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This work is licensed under a Creative Commons Attribution 4.0 International License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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