Agmatine ameliorates high glucose-induced neuronal cell senescence by regulating the p21 and p53 signaling

Juhyun Song, Byeori Lee, Somang Kang, Yumi Oh, Eosu Kim, Chul Hoon Kim, Ho Taek Song, Jong Eun Lee

Research output: Contribution to journalArticlepeer-review

20 Citations (Scopus)


Neuronal senescence caused by diabetic neuropathy is considered a common complication of diabetes mellitus. Neuronal senescence leads to the secretion of pro-inflammatory cytokines, the production of reactive oxygen species, and the alteration of cellular homeostasis. Agmatine, which is biosynthesized by arginine decarboxylation, has been reported in previous in vitro to exert a protective effect against various stresses. In present study, agmatine attenuated the cell death and the expression of pro-inflammatory cytokines such as IL-6, TNF-alpha and CCL2 in high glucose in vitro conditions. Moreover, the senescence associated-β-galatosidase's activity in high glucose exposed neuronal cells was reduced by agmatine. Increased p21 and reduced p53 in high glucose conditioned cells were changed by agmatine. Ultimately, agmatine inhibits the neuronal cell senescence through the activation of p53 and the inhibition of p21. Here, we propose that agmatine may ameliorate neuronal cell senescence in hyperglycemia.

Original languageEnglish
Pages (from-to)24-32
Number of pages9
JournalExperimental Neurobiology
Issue number1
Publication statusPublished - 2016 Feb 1

Bibliographical note

Publisher Copyright:
© Experimental Neurobiology 2016.

All Science Journal Classification (ASJC) codes

  • Clinical Neurology
  • Cellular and Molecular Neuroscience


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