Agmatine Ameliorates High Glucose-Induced Neuronal Cell Senescence by Regulating the p21 and p53 Signaling.
Agmatine Ameliorates High Glucose-Induced Neuronal Cell Senescence by Regulating the p21 and p53 Signaling.
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DOI：
10.5607/en.2016.25.1.24
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发表时间：
2016-02
影响因子：
2.4
通讯作者：
Lee JE
中科院分区：
文献类型：
--
作者：
Song J;Lee B;Kang S;Oh Y;Kim E;Kim CH;Song HT;Lee JE
糖尿病神经病变引起的神经元衰老被认为是糖尿病的常见并发症。神经元衰老导致促炎细胞因子的分泌、活性氧的产生和细胞内稳态的改变。胍丁胺是由精氨酸脱羧合成的，在体外实验中有报道对各种应激具有保护作用。在目前的研究中，胍丁胺减弱了细胞死亡和促炎细胞因子如IL-6，TNF-α和CCL 2在体外高糖条件下的表达。胍丁胺可降低高糖暴露神经细胞衰老相关β-半乳糖苷酶的活性。胍丁胺可改变高糖条件下p21蛋白表达的增加和p53蛋白表达的减少。胍丁胺通过激活p53和抑制p21来抑制神经细胞衰老。在这里，我们提出胍丁胺可以改善神经细胞衰老的高血糖症。
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.