Ghrelin Protects against Dexamethasone-Induced INS-1 Cell Apoptosis via ERK and p38MAPK Signaling
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...
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| Main Authors: | , , , , , , |
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| Format: | Article |
| Language: | English |
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Wiley
2016-01-01
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| Series: | International Journal of Endocrinology |
| Online Access: | http://dx.doi.org/10.1155/2016/4513051 |
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| author | Chengshuo Zhang Le Li Bochao Zhao Ao Jiao Xin Li Ning Sun Jialin Zhang |
| author_facet | Chengshuo Zhang Le Li Bochao Zhao Ao Jiao Xin Li Ning Sun Jialin Zhang |
| author_sort | Chengshuo Zhang |
| collection | DOAJ |
| description | 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. |
| format | Article |
| id | doaj-art-94c8edfcc9174d70bd72b0ec520613ed |
| institution | Kabale University |
| issn | 1687-8337 1687-8345 |
| language | English |
| publishDate | 2016-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | International Journal of Endocrinology |
| spelling | doaj-art-94c8edfcc9174d70bd72b0ec520613ed2025-02-03T01:24:17ZengWileyInternational Journal of Endocrinology1687-83371687-83452016-01-01201610.1155/2016/45130514513051Ghrelin Protects against Dexamethasone-Induced INS-1 Cell Apoptosis via ERK and p38MAPK SignalingChengshuo Zhang0Le Li1Bochao Zhao2Ao Jiao3Xin Li4Ning Sun5Jialin Zhang6Hepatobiliary Surgery Department and Unit of Organ Transplantation, First Hospital of China Medical University, Shenyang 110001, ChinaHepatobiliary Surgery Department, Chifeng Municipal Hospital, Chifeng 024000, ChinaHepatobiliary Surgery Department and Unit of Organ Transplantation, First Hospital of China Medical University, Shenyang 110001, ChinaHepatobiliary Surgery Department and Unit of Organ Transplantation, First Hospital of China Medical University, Shenyang 110001, ChinaDepartment of General Surgery, Fourth Hospital of China Medical University, Shenyang 110032, ChinaHepatobiliary Surgery Department and Unit of Organ Transplantation, First Hospital of China Medical University, Shenyang 110001, ChinaHepatobiliary Surgery Department and Unit of Organ Transplantation, First Hospital of China Medical University, Shenyang 110001, ChinaGlucocorticoid 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.http://dx.doi.org/10.1155/2016/4513051 |
| spellingShingle | Chengshuo Zhang Le Li Bochao Zhao Ao Jiao Xin Li Ning Sun Jialin Zhang Ghrelin Protects against Dexamethasone-Induced INS-1 Cell Apoptosis via ERK and p38MAPK Signaling International Journal of Endocrinology |
| title | Ghrelin Protects against Dexamethasone-Induced INS-1 Cell Apoptosis via ERK and p38MAPK Signaling |
| title_full | Ghrelin Protects against Dexamethasone-Induced INS-1 Cell Apoptosis via ERK and p38MAPK Signaling |
| title_fullStr | Ghrelin Protects against Dexamethasone-Induced INS-1 Cell Apoptosis via ERK and p38MAPK Signaling |
| title_full_unstemmed | Ghrelin Protects against Dexamethasone-Induced INS-1 Cell Apoptosis via ERK and p38MAPK Signaling |
| title_short | Ghrelin Protects against Dexamethasone-Induced INS-1 Cell Apoptosis via ERK and p38MAPK Signaling |
| title_sort | ghrelin protects against dexamethasone induced ins 1 cell apoptosis via erk and p38mapk signaling |
| url | http://dx.doi.org/10.1155/2016/4513051 |
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