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Rosiglitazone prevents acute pancreatitis through inhibiting microRNA‑26a expression

  • Authors:
    • Yan Chen
    • Wei Xiang
    • Xiang Li
    • Daming Wang
    • Chunyan Qian
  • View Affiliations / Copyright

    Affiliations: Department of Emergency, The First People's Hospital of Changzhou, The Third Affiliated Hospital of Soochow University, Changzhou, Jiangsu 213003, P.R. China, Drug Clinical Trial Institution, The First People's Hospital of Changzhou, The Third Affiliated Hospital of Soochow University, Changzhou, Jiangsu 213003, P.R. China
    Copyright: © Chen et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 1246-1252
    |
    Published online on: June 26, 2019
       https://doi.org/10.3892/etm.2019.7711
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Abstract

The aim of the present study was to investigate the regulatory effect of rosiglitazone on the progression of acute pancreatitis (AP) and pancreas injury, and the underlying mechanism. An AP rat model was established using caerulein and validated by detection of amylase, lipase, tumor necrosis factor‑α (TNF‑α), interleukin‑6 (IL‑6) and transforming growth factor‑β (TGF‑β) serum levels. Pancreatic injury was assessed by pathological examination. The expression levels of microRNA (miR)‑26a in AP rats and AR42J cells were analyzed using reverse transcription‑quantitative PCR (RT‑qPCR). Luciferase reporter gene assay was applied for detecting whether miR‑26a bound to the target gene phosphatase and tensin homolog (PTEN). The regulatory effect of rosiglitazone on the PI3K/AKT signaling pathway was analyzed by western blot analysis. Results demonstrated that establishment of an AP model was successful with severe pancreas injury and classic AP phenotypes observed in rats. Increased serum expression of amylase, lipase, TNF‑α, IL‑6 and TGF‑β were observed in AP rats. Rosiglitazone pretreatment prevented AP progression through suppression of miR‑26a expression via binding to and degrading PTEN. Western blot analysis demonstrated that rosiglitazone blocked the PI3K/AKT signaling pathway through PTEN. In conclusion, it was determined that rosiglitazone prevented AP by downregulating miR‑26a via the PI3K/AKT signaling pathway.
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Copy and paste a formatted citation
Spandidos Publications style
Chen Y, Xiang W, Li X, Wang D and Qian C: Rosiglitazone prevents acute pancreatitis through inhibiting microRNA‑26a expression. Exp Ther Med 18: 1246-1252, 2019.
APA
Chen, Y., Xiang, W., Li, X., Wang, D., & Qian, C. (2019). Rosiglitazone prevents acute pancreatitis through inhibiting microRNA‑26a expression. Experimental and Therapeutic Medicine, 18, 1246-1252. https://doi.org/10.3892/etm.2019.7711
MLA
Chen, Y., Xiang, W., Li, X., Wang, D., Qian, C."Rosiglitazone prevents acute pancreatitis through inhibiting microRNA‑26a expression". Experimental and Therapeutic Medicine 18.2 (2019): 1246-1252.
Chicago
Chen, Y., Xiang, W., Li, X., Wang, D., Qian, C."Rosiglitazone prevents acute pancreatitis through inhibiting microRNA‑26a expression". Experimental and Therapeutic Medicine 18, no. 2 (2019): 1246-1252. https://doi.org/10.3892/etm.2019.7711
Copy and paste a formatted citation
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Spandidos Publications style
Chen Y, Xiang W, Li X, Wang D and Qian C: Rosiglitazone prevents acute pancreatitis through inhibiting microRNA‑26a expression. Exp Ther Med 18: 1246-1252, 2019.
APA
Chen, Y., Xiang, W., Li, X., Wang, D., & Qian, C. (2019). Rosiglitazone prevents acute pancreatitis through inhibiting microRNA‑26a expression. Experimental and Therapeutic Medicine, 18, 1246-1252. https://doi.org/10.3892/etm.2019.7711
MLA
Chen, Y., Xiang, W., Li, X., Wang, D., Qian, C."Rosiglitazone prevents acute pancreatitis through inhibiting microRNA‑26a expression". Experimental and Therapeutic Medicine 18.2 (2019): 1246-1252.
Chicago
Chen, Y., Xiang, W., Li, X., Wang, D., Qian, C."Rosiglitazone prevents acute pancreatitis through inhibiting microRNA‑26a expression". Experimental and Therapeutic Medicine 18, no. 2 (2019): 1246-1252. https://doi.org/10.3892/etm.2019.7711
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