Ghrelin Protects against Dexamethasone-Induced INS-1 Cell Apoptosis via ERK and p38MAPK Signaling.
Ghrelin Protects against Dexamethasone-Induced INS-1 Cell Apoptosis via ERK and p38MAPK Signaling.
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Ghrelin 通过 ERK 和 p38MAPK 信号传导防止地塞米松诱导的 INS-1 细胞凋亡
DOI：
10.1155/2016/4513051
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发表时间：
2016
影响因子：
2.8
通讯作者：
Zhang J
中科院分区：
文献类型：
--
作者：
Zhang C;Li L;Zhao B;Jiao A;Li X;Sun N;Zhang J
糖皮质激素过量诱导胰岛细胞凋亡，这可能导致糖尿病。本研究探讨ghrelin对地塞米松诱导的INS-1细胞凋亡的保护作用。我们的数据显示，ghrelin（0.1 μM）抑制地塞米松（0.1 μM）诱导的INS-1细胞凋亡，并促进细胞增殖。此外，ghrelin上调Bcl-2表达，下调Bax表达，并降低caspase-3活性。Ghrelin对地塞米松诱导的INS-1细胞凋亡的保护作用通过生长激素促分泌素受体1a介导。进一步的研究表明，地塞米松处理后，ghrelin增加ERK的激活，降低p38 MAPK的表达。使用ERK抑制剂U 0126（10 μM）减弱Ghrelin介导的地塞米松诱导的INS-1细胞凋亡保护作用，使用p38 MAPK抑制剂SB 203580（10 μM）增加细胞活力。结论：Ghrelin对地塞米松诱导的INS-1细胞凋亡具有保护作用，其机制可能部分通过GHS-R1 a和ERK、p38 MAPK信号通路实现。
Glucocorticoid excess induces apoptosis of islet cells, which may result in diabetes. In this study, we investigated the protective effect of ghrelin on dexamethasone-induced INS-1 cell apoptosis. Our data showed that ghrelin (0.1 μM) inhibited dexamethasone-induced (0.1 μM) apoptosis of INS-1 cells and facilitated cell proliferation. Moreover, ghrelin upregulated Bcl-2 expression, downregulated Bax expression, and decreased caspase-3 activity. The protective effect of ghrelin against dexamethasone-induced INS-1 cell apoptosis was mediated via growth hormone secretagogue receptor 1a. Further studies revealed that ghrelin increased ERK activation and decreased p38MAPK expression after dexamethasone treatment. Ghrelin-mediated protection of dexamethasone-induced apoptosis of INS-1 cells was attenuated using the ERK inhibitor U0126 (10 μM), and cell viability increased using the p38MAPK inhibitor SB203580 (10 μM). In conclusion, ghrelin could protect against dexamethasone-induced INS-1 cell apoptosis, at least partially via GHS-R1a and the signaling pathway of ERK and p38MAPK.