Agmatine Ameliorates High Glucose-Induced Neuronal Cell Senescence by Regulating the p21 and p53 Signaling.
- Author:
Juhyun SONG
1
;
Byeori LEE
;
Somang KANG
;
Yumi OH
;
Eosu KIM
;
Chul Hoon KIM
;
Ho Taek SONG
;
Jong Eun LEE
Author Information
- Publication Type:In Vitro ; Original Article
- Keywords: Agmatine; High glucose; Hyperglycemia; Cell death; Senescence; Pro-inflammatory cytokines; p53; p21
- MeSH: Aging; Agmatine*; Arginine; Cell Aging*; Cell Death; Cytokines; Decarboxylation; Diabetes Mellitus; Diabetic Neuropathies; Glucose; Homeostasis; Hyperglycemia; Interleukin-6; Neurons*; Reactive Oxygen Species; Tumor Necrosis Factor-alpha
- From:Experimental Neurobiology 2016;25(1):24-32
- CountryRepublic of Korea
- Language:English
- Abstract: 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-beta-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.
