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Polydatin Alleviates Septic Myocardial Injury by Promoting SIRT6-Mediated Autophagy.

Xiaoyan Yuan1,2, Guo Chen1, Dongfeng Guo3

  • 1Department of Emergency Medicine, Shanghai Gongli Hospital, 219 Miao-Pu Road, Shanghai, 200135, China.

Inflammation
|May 13, 2020
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Summary

Polydatin (PD) protects against sepsis-induced heart damage by boosting sirtuin 6 (SIRT6)-mediated autophagy. This natural compound alleviates myocardial apoptosis and inflammation, offering potential therapeutic benefits for septic cardiomyopathy.

Keywords:
SIRT6autophagymyocardial injurypolydatinsepsis

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Area of Science:

  • Cardiology
  • Biochemistry
  • Pharmacology

Background:

  • Sepsis is a critical condition leading to organ damage, including the heart.
  • Polydatin (PD), a natural compound, exhibits antioxidant and anti-inflammatory effects.
  • The precise mechanism of PD's protection against sepsis-induced myocardial injury remains to be fully elucidated.

Purpose of the Study:

  • To investigate the protective effects and underlying mechanisms of Polydatin (PD) on sepsis-induced acute myocardial damage.
  • To explore the role of PD-upregulated sirtuin 6 (SIRT6) in mitigating myocardial injury.
  • To examine the involvement of autophagy in PD's cardioprotective actions.

Main Methods:

  • Utilized lipopolysaccharide (LPS)-induced H9c2 cells and a cecal ligation and puncture (CLP)-induced rat sepsis model.
  • Employed techniques including ELISA, western blotting, immunofluorescence, immunohistochemistry, and flow cytometry.
  • Investigated the effects of PD pretreatment, SIRT6 modulation, and autophagy inhibition (3-Methyladenine).

Main Results:

  • PD pretreatment significantly suppressed LPS-induced apoptosis in H9c2 cells and myocardial apoptosis in CLP-induced sepsis.
  • PD treatment upregulated SIRT6 expression and promoted autophagy, which was crucial for its protective effect.
  • PD reduced the expression of inflammatory factors (TNF-α, IL-1β, IL-6) in septic conditions.
  • Inhibition of SIRT6 or autophagy reversed the cardioprotective effects of PD.

Conclusions:

  • Polydatin (PD) demonstrates significant therapeutic potential in alleviating sepsis-induced myocardial injury.
  • PD exerts its cardioprotective effects primarily by promoting SIRT6-mediated autophagy.
  • The findings highlight PD as a promising agent for managing septic cardiomyopathy.