2. Academic Validation
  3. Dexmedetomidine-mediated regulation of miR-17-3p in H9C2 cells after hypoxia/reoxygenation injury

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

  • Exp Ther Med. 2020 Aug;20(2):917-925. doi: 10.3892/etm.2020.8775.
Tianhui Yuan 1 2 3,  Zhongqi Yang 1 2 3,  Shaoxiang Xian 4,  Yang Chen 5,  Lingjun Wang 6,  Weitao Chen 7,  Wenjie Long 8,  Yuanyuan Che 9
Affiliations

Affiliations

  • 1 Department of Drug Clinical Trials, The First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510405, P.R. China.
  • 2 Clinical Research Unit, The First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510405, P.R. China.
  • 3 Phase I Program, The First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510405, P.R. China.
  • 4 Department of Chinese Internal Medicine, The First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510405, P.R. China.
  • 5 School of Pharmaceuticals, The First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510405, P.R. China.
  • 6 Lingnan Medical Center, The First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510405, P.R. China.
  • 7 Intensive Care Unit, The First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510405, P.R. China.
  • 8 College of First Clinical Medicine, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510405, P.R. China.
  • 9 Department of Cardiology, Zaozhuang Municipal Hospital, Zaozhuang, Shandong 277102, P.R. China.
PMID: 32742334 DOI: 10.3892/etm.2020.8775
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.

Keywords

H9C2; dexmedetomidine; hypoxia/reoxygenation; microRNA-17-3p.

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