Sanguinarine attenuates hypoxia/reoxygenation-triggered H9c2 cell injury through activation of the Nrf2/NLRP3 pathway

DOI
  • Qiu Bo
    Department of Cardiovascular Medicine, Chongqing Red Cross Hospital (Jiangbei District People’s Hospital)
  • Li Xin
    Department of Cardiovascular Medicine, Chongqing Red Cross Hospital (Jiangbei District People’s Hospital)
  • Wang Wenna
    Department of Cardiovascular Medicine, Chongqing Red Cross Hospital (Jiangbei District People’s Hospital)

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説明

<p>Myocardial ischemia/reperfusion injury (MI/RI) is a prevalent condition encountered by many patients with ischemic heart disease, which can badly influence the health of patients and even do harm their lives. Sanguinarine (SA), one active ingredient separated from the poppy family, and exhibits anti-oxidant, anti-tumor, and anti-inflammation properties. However, the precise regulatory impacts and associated mechanisms of SA in the progression of MI/RI remain largely elusive. In this study, firstly, H9c2 cells were treated by hypoxia/reoxygenation (HR) to mimic MI/RI cell model. It was uncovered that SA strengthened HR-mediated cell viability of H9c2 cells. Following HR treatment, there was an increase in the production of inflammatory markers (TNF-α, IL-1β, and IL-6), whereas this effect was mitigated after SA ‍treatment. The oxidative stress was heightened after HR treatment, but this phenomenon was offset after SA treatment. SA activated the Nrf2/NLRP3 pathway and relieved proptosis. At ‍last, through rescue assays, it was demonstrated that SA improved HR-triggered inflammation and oxidative stress through Nrf2 pathway. SA also modulated HR-triggered cell viability, inflammation, and oxidative stress in rat primary cardiomyocytes. In summary, our findings indicate that SA protects against HR-induced H9c2 cell injury through activation of the Nrf2/NLRP3 pathway. This discovery suggests that SA may be one helpful drug for ameliorating MI/RI.</p>

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詳細情報 詳細情報について

  • CRID
    1390022457805564544
  • DOI
    10.3164/jcbn.24-235
  • ISSN
    18805086
    09120009
  • 本文言語コード
    en
  • データソース種別
    • JaLC
  • 抄録ライセンスフラグ
    使用不可

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