Dexmedetomidine protects PC12 cells from oxidative damage through regulation of miR-199a/HIF-1α
Background Although dexmedetomidine (Dex) has a significant neuroprotective effect in various nerve-damage models, the exact mechanism of which Dex protects cells from oxidative damage is not fully clear. This article recommended the protective effect of Dex on oxidative damage in PC12 cells.Methods...
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| Format: | Article |
| Language: | English |
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Taylor & Francis Group
2020-01-01
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| Series: | Artificial Cells, Nanomedicine, and Biotechnology |
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| Online Access: | https://www.tandfonline.com/doi/10.1080/21691401.2020.1716780 |
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| author | Ling Wu Yalin Xi Qinglong Kong |
| author_facet | Ling Wu Yalin Xi Qinglong Kong |
| author_sort | Ling Wu |
| collection | DOAJ |
| description | Background Although dexmedetomidine (Dex) has a significant neuroprotective effect in various nerve-damage models, the exact mechanism of which Dex protects cells from oxidative damage is not fully clear. This article recommended the protective effect of Dex on oxidative damage in PC12 cells.Methods The PC12 cells were incubated by hydrogen peroxide (H2O2) for 24 h and pre-treated by Dex for 30 min. Cell viability, apoptosis, HIF-1α expression and ROS level were detected by CCK-8, apoptosis assay, Western blot and ROS assay, respectively. The miR-199a expression was tested by qRT-PCR. Targeting relationship between miR-199a and HIF-1α was performed by dual luciferase activity assay. The activation of PI3K/AKT/mTOR and Wnt/β-catenin pathways was tested by western blot.Results Dex attenuated H2O2-induced oxidative damage, including the decline of cell viability, the raise of apoptosis and the generation of ROS in PC12 cells by down-regulating miR-199a expression. Moreover, Dex up-regulated HIF-1α expression via decreasing miR-199a level in PC12 cells and miR-199a targeted the 3′-UTR of HIF-1α. In addition, Dex activated PI3K/AKT/mTOR and Wnt/β-catenin pathways by declining miR-199a level.Conclusions This article illustrated the protective effect of Dex on oxidative damage in PC12 cells. Furthermore, Dex prevented PC12 cells from oxidative injury through the regulation of miR-199a/HIF-1α. |
| first_indexed | 2024-03-13T01:41:06Z |
| format | Article |
| id | doaj.art-cd905d2199fb4d88bf50dd189adce960 |
| institution | Directory Open Access Journal |
| issn | 2169-1401 2169-141X |
| language | English |
| last_indexed | 2025-03-21T05:46:34Z |
| publishDate | 2020-01-01 |
| publisher | Taylor & Francis Group |
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| series | Artificial Cells, Nanomedicine, and Biotechnology |
| spelling | doaj.art-cd905d2199fb4d88bf50dd189adce9602024-07-23T18:44:31ZengTaylor & Francis GroupArtificial Cells, Nanomedicine, and Biotechnology2169-14012169-141X2020-01-0148150651410.1080/21691401.2020.1716780Dexmedetomidine protects PC12 cells from oxidative damage through regulation of miR-199a/HIF-1αLing Wu0Yalin Xi1Qinglong Kong2Department of Clinical Pharmacy, Dalian Central Hospital, Dalian, ChinaDepartment of Clinical Pharmacy, Dalian Central Hospital, Dalian, ChinaDepartment of Thoracic Surgery, Dalian Central Hospital, Dalian, ChinaBackground Although dexmedetomidine (Dex) has a significant neuroprotective effect in various nerve-damage models, the exact mechanism of which Dex protects cells from oxidative damage is not fully clear. This article recommended the protective effect of Dex on oxidative damage in PC12 cells.Methods The PC12 cells were incubated by hydrogen peroxide (H2O2) for 24 h and pre-treated by Dex for 30 min. Cell viability, apoptosis, HIF-1α expression and ROS level were detected by CCK-8, apoptosis assay, Western blot and ROS assay, respectively. The miR-199a expression was tested by qRT-PCR. Targeting relationship between miR-199a and HIF-1α was performed by dual luciferase activity assay. The activation of PI3K/AKT/mTOR and Wnt/β-catenin pathways was tested by western blot.Results Dex attenuated H2O2-induced oxidative damage, including the decline of cell viability, the raise of apoptosis and the generation of ROS in PC12 cells by down-regulating miR-199a expression. Moreover, Dex up-regulated HIF-1α expression via decreasing miR-199a level in PC12 cells and miR-199a targeted the 3′-UTR of HIF-1α. In addition, Dex activated PI3K/AKT/mTOR and Wnt/β-catenin pathways by declining miR-199a level.Conclusions This article illustrated the protective effect of Dex on oxidative damage in PC12 cells. Furthermore, Dex prevented PC12 cells from oxidative injury through the regulation of miR-199a/HIF-1α.https://www.tandfonline.com/doi/10.1080/21691401.2020.1716780PC12 cellsdexmedetomidineoxidative damagemiR-199aHIF-1α |
| spellingShingle | Ling Wu Yalin Xi Qinglong Kong Dexmedetomidine protects PC12 cells from oxidative damage through regulation of miR-199a/HIF-1α Artificial Cells, Nanomedicine, and Biotechnology PC12 cells dexmedetomidine oxidative damage miR-199a HIF-1α |
| title | Dexmedetomidine protects PC12 cells from oxidative damage through regulation of miR-199a/HIF-1α |
| title_full | Dexmedetomidine protects PC12 cells from oxidative damage through regulation of miR-199a/HIF-1α |
| title_fullStr | Dexmedetomidine protects PC12 cells from oxidative damage through regulation of miR-199a/HIF-1α |
| title_full_unstemmed | Dexmedetomidine protects PC12 cells from oxidative damage through regulation of miR-199a/HIF-1α |
| title_short | Dexmedetomidine protects PC12 cells from oxidative damage through regulation of miR-199a/HIF-1α |
| title_sort | dexmedetomidine protects pc12 cells from oxidative damage through regulation of mir 199a hif 1α |
| topic | PC12 cells dexmedetomidine oxidative damage miR-199a HIF-1α |
| url | https://www.tandfonline.com/doi/10.1080/21691401.2020.1716780 |
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