Protective effect of Guanxin Danshen formula on myocardial ischemiareperfusion injury in rats

Lanfang Li1, Bo Liu1, Min Wang1

  • 1Institute of Medicinal Plant Development - Peking Union Medical College and Chinese Academy of Medical Sciences - Beijing, China.

Abstract

Insights

Guanxin Danshen formula (GXDSF) protects against myocardial ischemia/reperfusion injury (MIRI) in rats. It reduces inflammation and cell death by targeting the NLRP3 inflammasome pathway, preserving heart tissue.

Area of Science:

  • Cardiovascular Research
  • Pharmacology
  • Cellular Biology

Background:

  • Myocardial ischemia/reperfusion injury (MIRI) causes significant myocardial tissue necrosis, increasing infarct size.
  • Understanding protective mechanisms against MIRI is crucial for improving patient outcomes.

Purpose of the Study:

  • To investigate the protective effects of Guanxin Danshen formula (GXDSF) on MIRI in a rat model.
  • To elucidate the underlying mechanism of GXDSF's cardioprotective action.

Main Methods:

  • Establishment of MIRI model in rats and a H9C2 cardiomyocyte hypoxia-reoxygenation injury model.
  • Assessment of cardiac function, myocardial structural integrity, serum inflammatory markers, and oxidative stress indicators.
  • Analysis of key protein expression, including NLRP3 inflammasome components (NLRP3, caspase-1, GSDMD) and cytokines (IL-1β, IL-6, TNF-α).

Main Results:

  • GXDSF significantly reduced myocardial infarct size and structural damage in MIRI rats.
  • Treatment decreased serum levels of IL-1β and IL-6, myocardial enzyme activity, and increased superoxide dismutase (SOD) activity.
  • GXDSF suppressed the expression of NLRP3, IL-1β, caspase-1, and GSDMD in myocardial tissue and H9C2 cells.

Conclusions:

  • GXDSF demonstrates significant cardioprotective effects against MIRI in rats.
  • The formula alleviates myocardial inflammation and oxidative stress by modulating the NLRP3 inflammasome pathway.
  • GXDSF improves myocardial structure and reduces infarct size, offering a potential therapeutic strategy for MIRI.

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