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Tranilast reduces cardiomyocyte injury induced by ischemia‑reperfusion via Nrf2/HO‑1/NF‑κB signaling

  • Authors:
    • Wei Wang
    • Qifeng Shen
  • View Affiliations / Copyright

    Affiliations: Quality Management Office, Zhejiang Sian International Hospital, Jiaxing, Zhejiang 314000, P.R. China, Department of Cardiovascular Diseases, Zhejiang Sian International Hospital, Jiaxing, Zhejiang 314000, P.R. China
    Copyright: © Wang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Article Number: 160
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    Published online on: February 22, 2023
       https://doi.org/10.3892/etm.2023.11859
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Abstract

Tranilast, a synthetic derivative of a tryptophan metabolite, can be used to treat heart diseases. However, the specific mechanism underlying the effect of tranilast on ischemia‑reperfusion (I/R) injury‑induced cardiomyocyte apoptosis remains unclear. Therefore, the present study aimed to determine if tranilast could attenuate I/R‑induced cardiomyocyte injury. A hypoxia/reoxygenation (H/R) model of H9c2 cardiomyocytes was established to simulate I/R‑induced cardiomyocyte injury. The viability, apoptosis, inflammation and oxidative stress in H/R‑induced H9c2 cells following treatment with tranilast were evaluated by Cell Counting Kit‑8 and TUNEL assay. Commercially available kits were used to detect the levels of inflammatory markers and oxidative stress indicators. In addition, the expression levels of the apoptosis‑ and nuclear factor erythroid 2‑related factor 2 (Nrf2)/heme oxygenase‑1 (HO‑1)/NF‑κB signalling pathway‑associated proteins were detected by western blotting. The levels of reactive oxygen species were determined using 2',7'‑dichlorofluorescin diacetate assay kit. The viability of H9c2 cells was decreased following induction with H/R. However, treatment with tranilast increased viability while decreasing apoptosis, oxidative stress and inflammatory response in H/R‑induced H9c2 cells by activating Nrf2/HO‑1/NF‑κB signalling. Furthermore, treatment with ML‑385, an Nrf2 inhibitor, reversed the effects of tranilast on H/R‑induced H9c2 cells. In conclusion, the results of the present study suggested that tranilast could attenuate I/R‑induced cardiomyocyte injury via the Nrf2/HO‑1/NF‑κB signalling pathway.
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Copy and paste a formatted citation
Spandidos Publications style
Wang W and Shen Q: Tranilast reduces cardiomyocyte injury induced by ischemia‑reperfusion via Nrf2/HO‑1/NF‑κB signaling. Exp Ther Med 25: 160, 2023.
APA
Wang, W., & Shen, Q. (2023). Tranilast reduces cardiomyocyte injury induced by ischemia‑reperfusion via Nrf2/HO‑1/NF‑κB signaling. Experimental and Therapeutic Medicine, 25, 160. https://doi.org/10.3892/etm.2023.11859
MLA
Wang, W., Shen, Q."Tranilast reduces cardiomyocyte injury induced by ischemia‑reperfusion via Nrf2/HO‑1/NF‑κB signaling". Experimental and Therapeutic Medicine 25.4 (2023): 160.
Chicago
Wang, W., Shen, Q."Tranilast reduces cardiomyocyte injury induced by ischemia‑reperfusion via Nrf2/HO‑1/NF‑κB signaling". Experimental and Therapeutic Medicine 25, no. 4 (2023): 160. https://doi.org/10.3892/etm.2023.11859
Copy and paste a formatted citation
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Spandidos Publications style
Wang W and Shen Q: Tranilast reduces cardiomyocyte injury induced by ischemia‑reperfusion via Nrf2/HO‑1/NF‑κB signaling. Exp Ther Med 25: 160, 2023.
APA
Wang, W., & Shen, Q. (2023). Tranilast reduces cardiomyocyte injury induced by ischemia‑reperfusion via Nrf2/HO‑1/NF‑κB signaling. Experimental and Therapeutic Medicine, 25, 160. https://doi.org/10.3892/etm.2023.11859
MLA
Wang, W., Shen, Q."Tranilast reduces cardiomyocyte injury induced by ischemia‑reperfusion via Nrf2/HO‑1/NF‑κB signaling". Experimental and Therapeutic Medicine 25.4 (2023): 160.
Chicago
Wang, W., Shen, Q."Tranilast reduces cardiomyocyte injury induced by ischemia‑reperfusion via Nrf2/HO‑1/NF‑κB signaling". Experimental and Therapeutic Medicine 25, no. 4 (2023): 160. https://doi.org/10.3892/etm.2023.11859
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