Agmatine Ameliorates High Glucose-Induced Neuronal Cell Senescence by Regulating the p21 and p53 Signaling
| Autor: | Juhyun Song, Eosu Kim, Chul Hoon Kim, Jong Eun Lee, Somang Kang, Yumi Oh, Byeori Lee, Ho Taek Song |
|---|---|
| Rok vydání: | 2016 |
| Předmět: |
Cell death
p53 0301 basic medicine Senescence medicine.medical_specialty Programmed cell death Agmatine Arginine Pro-inflammatory cytokines Cell Cellular homeostasis Biology Proinflammatory cytokine 03 medical and health sciences Cellular and Molecular Neuroscience chemistry.chemical_compound 0302 clinical medicine Internal medicine medicine chemistry.chemical_classification Reactive oxygen species p21 Cell biology 030104 developmental biology medicine.anatomical_structure Endocrinology chemistry Hyperglycemia Original Article Neurology (clinical) High glucose 030217 neurology & neurosurgery |
| Zdroj: | Experimental Neurobiology |
| ISSN: | 2093-8144 1226-2560 |
| DOI: | 10.5607/en.2016.25.1.24 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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