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Geniposide protects against sepsis-induced myocardial dysfunction through AMPKα-dependent pathway
Peng Song1, Di-Fei Shen1, Yan-Yan Meng1
1Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, 430060, PR China; Hubei Key Laboratory of Metabolic and Chronic Diseases, Wuhan, 430060, PR China.
Free Radical Biology & Medicine
|February 22, 2020
Summary
Geniposide (GE) protects against sepsis-induced heart dysfunction by activating AMPKα, which reduces inflammation and cell death. This study reveals GE
Area of Science:
- Cardiology
- Pharmacology
- Molecular Biology
Background:
- Sepsis-induced myocardial dysfunction involves inflammation and cardiomyocyte loss.
- Geniposide (GE) previously showed cardioprotective effects against obesity-induced inflammation.
- The impact of GE on sepsis-related cardiac dysfunction remained unexplored.
Purpose of the Study:
- To investigate the protective effects of geniposide (GE) against lipopolysaccharide (LPS)-induced myocardial dysfunction in mice.
- To elucidate the underlying molecular mechanisms involving AMP-activated protein kinase α (AMPKα) and the NLRP3 inflammasome.
Main Methods:
- Mice were treated with LPS to induce sepsis and subsequently with GE (50 mg/kg) for 7 days.
- Cardiac function, survival rates, inflammatory markers, and cardiomyocyte apoptosis/pyroptosis were assessed.
- Experiments involved wild-type, NOD-like receptor protein 3 (NLRP3)-deficient, and AMPKα-knockout mice.
Main Results:
- GE treatment significantly improved survival and cardiac function in LPS-induced sepsis.
- GE suppressed myocardial inflammation, reactive oxygen species (ROS) accumulation, and cardiomyocyte loss.
- These protective effects were dependent on NLRP3 inflammasome and AMPKα activation, with GE reducing p47phox.
- GE restored AMPKα phosphorylation and activity in sepsis-induced hearts.
Conclusions:
- Geniposide (GE) ameliorates sepsis-induced myocardial dysfunction by activating AMPKα.
- AMPKα activation by GE suppresses ROS accumulation, thereby inhibiting NLRP3 inflammasome-mediated cardiomyocyte apoptosis and pyroptosis.
- GE represents a potential therapeutic agent for sepsis-related cardiac complications.
