Obeticholic Acid Inhibit Mitochondria Dysfunction Via Regulating ERK1/2-DRP Pathway to Exert Protective Effect on Lipopolysaccharide-Induced Myocardial Injury
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View abstract on PubMed
Summary
This summary is machine-generated.Obeticholic acid (OCA), an FXR agonist, protects against sepsis-induced myocardial injury by improving mitochondrial function and reducing oxidative stress. OCA inhibits the ERK1/2-DRP pathway, offering a potential therapeutic strategy for sepsis-associated heart damage.
Area Of Science
- Cardiovascular Physiology
- Mitochondrial Biology
- Pharmacology
Background
- Farnesoid X receptor (FXR) is crucial in cardiovascular health and disease.
- The protective effects and mechanisms of FXR agonist obeticholic acid (OCA) in sepsis-induced myocardial injury are not well understood.
Purpose Of The Study
- To investigate the protective role of OCA against lipopolysaccharide (LPS)-induced myocardial injury in mice.
- To elucidate the underlying mechanisms, focusing on mitochondrial function and the ERK signaling pathway.
Main Methods
- Mice were pretreated with OCA before LPS administration.
- Cardiac histopathology, FXR expression, and mitochondrial function were assessed.
- In vitro studies used H9c2 cells and primary cardiomyocytes with OCA and an ERK inhibitor (PD98059).
Main Results
- OCA pretreatment significantly ameliorated LPS-induced myocardial injury.
- OCA reduced reactive oxygen species (ROS) and preserved mitochondrial membrane potential (ΔΨm).
- OCA upregulated antioxidant enzymes (GPX1, SOD1, SOD2, NRF-2), improved mitochondrial respiration (Complex I), and inhibited the ERK1/2-DRP pathway.
Conclusions
- FXR agonist OCA confers protection against sepsis-associated myocardial injury.
- OCA exerts its protective effects by mitigating mitochondrial dysfunction and oxidative stress via the ERK1/2-DRP signaling pathway.
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