Open Access

Dexmedetomidine‑mediated regulation of miR‑17‑3p in H9C2 cells after hypoxia/reoxygenation injury

  • Authors:
    • Tianhui Yuan
    • Zhongqi Yang
    • Shaoxiang Xian
    • Yang Chen
    • Lingjun Wang
    • Weitao Chen
    • Wenjie Long
    • Yuanyuan Che
  • View Affiliations

  • Published online on: May 20, 2020     https://doi.org/10.3892/etm.2020.8775
  • Pages: 917-925
  • Copyright: © Yuan et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Patients with heart disease often suffer from ischemia, which can be treated by reperfusion. However, this treatment can lead to the development of ischemia/reperfusion (I/R) injury, an inflammatory condition that can cause further heart damage. Dexmedetomidine (Dex), an α2‑adrenoceptor agonist, and the microRNA (miR)‑17‑3p, have both been suggested to alleviate I/R injury and cardiac tissue inflammation. The aim of the present study was to investigate whether Dex and miR‑17‑3p could act together to prevent I/R injury. H9C2 cells, a myoblast cell line used as a model of rat cardiomyocytes, were cultured in a hypoxic environment for 3 h, and then reoxygenated for 3 h. This hypoxia/reoxygenation (H/R) was used to model I/R. Cell Counting kit‑8 was used to determine cell viability and an annexin V‑FITC/propidium iodide apoptosis kit used to analyze cell apoptosis. A dual luciferase reporter assay was used to determine the interaction between miR‑17‑3p and toll‑like receptor 4 (TLR4). Western blotting and reverse transcription‑quantitative PCR were used to determine protein levels and mRNA expression of TLR4 and galectin‑3. A concentration of 0.1‑10 µmol/l Dex attenuated H/R injury, which was accompanied by increased miR‑17‑3p levels. Additionally, the inhibition of miR‑17‑3p exacerbated H/R injury and reduced the effect of Dex on H/R injury. H/R led to an increased galectin‑3 level compared with that in control cells, and Dex or miR‑17‑3p inhibitor did not markedly affect the level of galectin‑3, indicating that Dex alleviated the effects of I/R injury through other pathways. Inhibition of miR‑17‑3p in Dex‑induced H9C2 cells during H/R increased the expression of inflammatory mediators including tumor necrosis factor‑α, interleukin (IL)‑6, IL‑1β and phosphorylated NFκB subunit p65, while Dex reduced the H/R‑induced expression of these inflammatory mediators. Inhibition of TLR4 also attenuated H/R injury. In summary, the findings of the present study indicated that Dex reduced H/R injury in H9C2 cell via the modulation of inflammatory signaling pathways, and these inflammatory factors could be regulated by miR‑17‑3p.

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August-2020
Volume 20 Issue 2

Print ISSN: 1792-0981
Online ISSN:1792-1015

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APA
Yuan, T., Yang, Z., Xian, S., Chen, Y., Wang, L., Chen, W. ... Che, Y. (2020). Dexmedetomidine‑mediated regulation of miR‑17‑3p in H9C2 cells after hypoxia/reoxygenation injury. Experimental and Therapeutic Medicine, 20, 917-925. https://doi.org/10.3892/etm.2020.8775
MLA
Yuan, T., Yang, Z., Xian, S., Chen, Y., Wang, L., Chen, W., Long, W., Che, Y."Dexmedetomidine‑mediated regulation of miR‑17‑3p in H9C2 cells after hypoxia/reoxygenation injury". Experimental and Therapeutic Medicine 20.2 (2020): 917-925.
Chicago
Yuan, T., Yang, Z., Xian, S., Chen, Y., Wang, L., Chen, W., Long, W., Che, Y."Dexmedetomidine‑mediated regulation of miR‑17‑3p in H9C2 cells after hypoxia/reoxygenation injury". Experimental and Therapeutic Medicine 20, no. 2 (2020): 917-925. https://doi.org/10.3892/etm.2020.8775