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Sevoflurane Alleviates Hypoxia/Reoxygenation-Induced Myocardial Injury by Regulating miR-300: An In Vitro Study.

Chenyu Wang1, Zhenyun Tao1, Shuai Wang1

  • 1Department of Anesthesiology, Yiwu Central Hospital, Yiwu, China.

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Sevoflurane preconditioning protects the heart by upregulating miR-300, which targets HMGB1. This mechanism mitigates myocardial hypoxia/reoxygenation injury, offering a new therapeutic avenue for cardiovascular ischemia.

Keywords:
HMGB1Sevofluranehypoxia/reoxygenationmiR‐300myocardial ischemia/reperfusion injury

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Area of Science:

  • Cardiology
  • Molecular Biology
  • Anesthesiology

Background:

  • Sevoflurane (Sev) exhibits myocardial protective effects, but the underlying molecular mechanisms require further elucidation.
  • MicroRNA-300 (miR-300) has emerged as a potential mediator in cellular responses to stress.
  • Understanding the role of miR-300 in sevoflurane-induced cardioprotection against hypoxia/reoxygenation (H/R) injury is crucial.

Purpose of the Study:

  • To investigate the functional role and mechanistic basis of miR-300 in sevoflurane-mediated cardioprotection against myocardial H/R injury.
  • To determine if miR-300 directly targets High-Mobility Group Box 1 (HMGB1).
  • To explore the therapeutic potential of modulating the miR-300/HMGB1 axis in cardiovascular ischemia/reperfusion injury.

Main Methods:

  • AC16 cardiomyocytes were preconditioned with sevoflurane and subjected to H/R.
  • Quantitative real-time PCR (qRT-PCR) was used to measure miR-300 and HMGB1 expression.
  • Cell viability, apoptosis, myocardial injury markers, inflammatory cytokines, and oxidative stress indicators were assessed using CCK-8, flow cytometry, ELISA, and commercial kits.
  • Dual-luciferase reporter assays confirmed the direct targeting of HMGB1 by miR-300.

Main Results:

  • Sevoflurane preconditioning attenuated H/R-induced cardiomyocyte injury, apoptosis, inflammation, and oxidative stress.
  • miR-300 expression decreased with prolonged hypoxia but was preserved by sevoflurane preconditioning.
  • miR-300 directly targets HMGB1, and HMGB1 knockdown reversed the negative impact of miR-300 downregulation on sevoflurane-mediated cardioprotection.

Conclusions:

  • miR-300 plays a critical role in mediating the cardioprotective effects of sevoflurane preconditioning against H/R injury.
  • The cardioprotection is achieved through the miR-300 targeting of HMGB1, thereby regulating myocardial injury.
  • This finding provides a novel theoretical basis for understanding and potentially treating cardiovascular ischemia/reperfusion injury.