Galanin Protects Rat Cortical Astrocyte from Oxidative Stress: Involvement of GalR2 and pERK1/2 Signal Pathway.
Galanin Protects Rat Cortical Astrocyte from Oxidative Stress: Involvement of GalR2 and pERK1/2 Signal Pathway.
复制标题
甘丙肽保护大鼠皮质星形胶质细胞免受氧化应激：GalR2 和 pERK1/2 信号通路的参与。
DOI：
10.1155/2019/2716028
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发表时间：
2019
影响因子：
4.6
通讯作者：
Xu Zhi-Qing David
中科院分区：
文献类型：
--
作者：
Sun Jing;Xu Shu;Li Hui;Li Liang;Xu Zhi-Qing David
已发现神经肽甘丙肽及其受体对神经元具有保护作用。然而，甘丙肽对星形胶质细胞的作用仍不清楚。本研究旨在探讨甘丙肽对H2 O2诱导的大鼠皮层星形胶质细胞氧化应激后活性的影响及其可能的受体和信号转导机制。甘丙肽处理对培养的皮质星形胶质细胞中H2 O2诱导的毒性具有显著的保护作用。H2 O2诱导星形胶质细胞磷酸化细胞外信号相关激酶1/2（pERK 1/2）上调，这被甘丙肽抑制，表明pERK 1/2信号通路参与甘丙肽的保护作用。在培养的皮质星形胶质细胞中，GalR 2的表达水平高于GalR 1和GalR 3，GalR 2激动剂AR-M1896模拟甘丙肽对星形胶质细胞的作用，这意味着甘丙肽的保护作用主要由GalR 2介导。同时，甘丙肽对大鼠皮层星形胶质细胞的A1型转化没有影响。所有这些结果表明，甘丙肽通过抑制H2 O2诱导的pERK 1/2上调（主要通过GalR 2）来保护大鼠皮质星形胶质细胞免受氧化应激。
The neuropeptide galanin and its receptors have been found to have protective effects on neurons. However, the role of galanin on astrocytes is still unclear. The present study is aimed at investigating the effects of galanin on the viability of cultured rat cortical astrocytes after oxidative stress induced by H2O2and possible receptor and signaling mechanisms involved. Treatment of galanin had significant protective effects against H2O2‐induced toxicity in the cultured cortical astrocytes. H2O2induced an upregulation of phosphorylated extracellular signal‐related kinase1/2 (pERK1/2) in astrocytes, which was suppressed by coapplication of galanin, suggesting an involvement of the pERK1/2 signal pathway in the protective effects of galanin. GalR2 has higher expression levels than GalR1 and GalR3 in the cultured cortical astrocytes, and GalR2 agonist AR‐M1896 mimicked galanin effects on the astrocytes, implying that galanin protective effects mainly mediated by GalR2. Meanwhile, galanin had no effect on the A1‐type transformation of rat cortical astrocytes. All those results suggest that galanin protects rat cortical astrocytes from oxidative stress by suppressing H2O2‐induced upregulation of pERK1/2, mainly through GalR2.