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Article

Sevoflurane preconditioning inhibits cardiomyocyte injury induced by oxygen‑glucose deprivation by modulating TXNIP

  • Authors:
    • Meina Ma
    • Rui Li
    • Wenbo Sun
    • Qi Wang
    • Hong Yu
    • Hongmei Yu
  • View Affiliations / Copyright

    Affiliations: Department of Anesthesiology, Cangzhou Central Hospital, Cangzhou, Hebei 061001, P.R. China
  • Pages: 889-897
    |
    Published online on: June 11, 2020
       https://doi.org/10.3892/ijmm.2020.4639
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Abstract

The thioredoxin interaction protein (TXNIP) has been reported to be closely related to cell oxidative stress, apoptosis and inflammation. TXNIP is involved in the regulation of oxidative stress in lung and renal injury. However, it is unclear as to whether it participates in the protective effects of sevoflurane preconditioning in cardiomyocyte injury caused by oxidative stress in ischemia. In the present study, H9c2 cardiomyocytes were cultured with 0, 1.5, 2, 3.5, 5 or 6% sevoflurane for 3 h, followed by exposure to oxygen and glucose deprivation. The results demonstrated that oxygen and glucose deprivation induced an increase in TXNIP expression, lactate dehydrogenase (LDH) release, caspase‑3 activity, reactive oxygen species and malondialdehyde production. Preconditioning of the H9c2 cells with 3.5% sevoflurane suppressed TXNIP expression, LDH leakage, caspase‑3 activity, reactive oxygen species and malondialdehyde production, and it promoted cell viability. TXNIP overexpression reversed the effects of 3.5% sevoflurane preconditioning on caspase‑3 activity, reactive oxygen production and cell viability. Furthermore, TXNIP modulated p27 expression via PKB (protein kinase B/AKT) phosphorylation following preconditioning with 3.5% sevoflurane, and oxygen and glucose deprivation. On the whole these findings indicated that sevoflurane preconditioning protected the H9c2 cells against injury induced by oxygen and glucose deprivation by modulating TXNIP, AKT activation and p27 signaling.
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Copy and paste a formatted citation
Spandidos Publications style
Ma M, Li R, Sun W, Wang Q, Yu H and Yu H: Sevoflurane preconditioning inhibits cardiomyocyte injury induced by oxygen‑glucose deprivation by modulating TXNIP. Int J Mol Med 46: 889-897, 2020.
APA
Ma, M., Li, R., Sun, W., Wang, Q., Yu, H., & Yu, H. (2020). Sevoflurane preconditioning inhibits cardiomyocyte injury induced by oxygen‑glucose deprivation by modulating TXNIP. International Journal of Molecular Medicine, 46, 889-897. https://doi.org/10.3892/ijmm.2020.4639
MLA
Ma, M., Li, R., Sun, W., Wang, Q., Yu, H., Yu, H."Sevoflurane preconditioning inhibits cardiomyocyte injury induced by oxygen‑glucose deprivation by modulating TXNIP". International Journal of Molecular Medicine 46.2 (2020): 889-897.
Chicago
Ma, M., Li, R., Sun, W., Wang, Q., Yu, H., Yu, H."Sevoflurane preconditioning inhibits cardiomyocyte injury induced by oxygen‑glucose deprivation by modulating TXNIP". International Journal of Molecular Medicine 46, no. 2 (2020): 889-897. https://doi.org/10.3892/ijmm.2020.4639
Copy and paste a formatted citation
x
Spandidos Publications style
Ma M, Li R, Sun W, Wang Q, Yu H and Yu H: Sevoflurane preconditioning inhibits cardiomyocyte injury induced by oxygen‑glucose deprivation by modulating TXNIP. Int J Mol Med 46: 889-897, 2020.
APA
Ma, M., Li, R., Sun, W., Wang, Q., Yu, H., & Yu, H. (2020). Sevoflurane preconditioning inhibits cardiomyocyte injury induced by oxygen‑glucose deprivation by modulating TXNIP. International Journal of Molecular Medicine, 46, 889-897. https://doi.org/10.3892/ijmm.2020.4639
MLA
Ma, M., Li, R., Sun, W., Wang, Q., Yu, H., Yu, H."Sevoflurane preconditioning inhibits cardiomyocyte injury induced by oxygen‑glucose deprivation by modulating TXNIP". International Journal of Molecular Medicine 46.2 (2020): 889-897.
Chicago
Ma, M., Li, R., Sun, W., Wang, Q., Yu, H., Yu, H."Sevoflurane preconditioning inhibits cardiomyocyte injury induced by oxygen‑glucose deprivation by modulating TXNIP". International Journal of Molecular Medicine 46, no. 2 (2020): 889-897. https://doi.org/10.3892/ijmm.2020.4639
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