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Article

Reduced mitochondrial response sensitivity is involved in the anti‑apoptotic effect of dexmedetomidine pretreatment in cardiomyocytes

  • Authors:
    • Xiaojian Weng
    • Xiaodan Zhang
    • Xiaofei Lu
    • Jin Wu
    • Shitong Li
  • View Affiliations / Copyright

    Affiliations: Department of Anesthesiology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200080, P.R. China, Department of Intensive Care Unit, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200080, P.R. China
  • Pages: 2328-2338
    |
    Published online on: January 12, 2018
       https://doi.org/10.3892/ijmm.2018.3384
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Abstract

Dexmedetomidine is a commonly used α2-adreno­ceptor agonist, which affects various organs, including providing beneficial effects on the heart. However, the mechanism underlying the cardiac benefit remains to be fully elucidated. In the present study, it was demonstrated that dexmedetomidine pretreatment on primary cultured rat cardiomyocytes protected against reactive oxygen species (ROS)‑induced apoptosis. In terms of the potential mechanism, it was demonstrated that dexmedetomidine inhibited mitochondrial biogenesis and mitochondrial respiratory complexes, but with increased coupling efficiency. However, dexmedetomidine upregulated mitochondrial membrane potential (Δψm) and resisted against the loss of Δψm induced by carbonilcyanide p‑triflouromethoxyphenylhydrazone. Due to the importance of mitochondria affecting ROS, the present study investigated the dexmedetomidine‑suppressed mitochondrial response to H2O2 stimulation, which was explained by suppressed ROS levels and the suppression of the increased oxygen consumption rate. Results demonstrated for the first time, to the best of our knowledge, a novel protective mechanism for dexmedetomidine on cardiomyocytes through the attenuated response of mitochondria towards H2O2, which had a protective effect against ROS‑induced apoptosis.
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Copy and paste a formatted citation
Spandidos Publications style
Weng X, Zhang X, Lu X, Wu J and Li S: Reduced mitochondrial response sensitivity is involved in the anti‑apoptotic effect of dexmedetomidine pretreatment in cardiomyocytes. Int J Mol Med 41: 2328-2338, 2018.
APA
Weng, X., Zhang, X., Lu, X., Wu, J., & Li, S. (2018). Reduced mitochondrial response sensitivity is involved in the anti‑apoptotic effect of dexmedetomidine pretreatment in cardiomyocytes. International Journal of Molecular Medicine, 41, 2328-2338. https://doi.org/10.3892/ijmm.2018.3384
MLA
Weng, X., Zhang, X., Lu, X., Wu, J., Li, S."Reduced mitochondrial response sensitivity is involved in the anti‑apoptotic effect of dexmedetomidine pretreatment in cardiomyocytes". International Journal of Molecular Medicine 41.4 (2018): 2328-2338.
Chicago
Weng, X., Zhang, X., Lu, X., Wu, J., Li, S."Reduced mitochondrial response sensitivity is involved in the anti‑apoptotic effect of dexmedetomidine pretreatment in cardiomyocytes". International Journal of Molecular Medicine 41, no. 4 (2018): 2328-2338. https://doi.org/10.3892/ijmm.2018.3384
Copy and paste a formatted citation
x
Spandidos Publications style
Weng X, Zhang X, Lu X, Wu J and Li S: Reduced mitochondrial response sensitivity is involved in the anti‑apoptotic effect of dexmedetomidine pretreatment in cardiomyocytes. Int J Mol Med 41: 2328-2338, 2018.
APA
Weng, X., Zhang, X., Lu, X., Wu, J., & Li, S. (2018). Reduced mitochondrial response sensitivity is involved in the anti‑apoptotic effect of dexmedetomidine pretreatment in cardiomyocytes. International Journal of Molecular Medicine, 41, 2328-2338. https://doi.org/10.3892/ijmm.2018.3384
MLA
Weng, X., Zhang, X., Lu, X., Wu, J., Li, S."Reduced mitochondrial response sensitivity is involved in the anti‑apoptotic effect of dexmedetomidine pretreatment in cardiomyocytes". International Journal of Molecular Medicine 41.4 (2018): 2328-2338.
Chicago
Weng, X., Zhang, X., Lu, X., Wu, J., Li, S."Reduced mitochondrial response sensitivity is involved in the anti‑apoptotic effect of dexmedetomidine pretreatment in cardiomyocytes". International Journal of Molecular Medicine 41, no. 4 (2018): 2328-2338. https://doi.org/10.3892/ijmm.2018.3384
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