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Cardamonin protects against lipopolysaccharide-induced myocardial contractile dysfunction in mice through
Ying Tan1,2,3, Hong-Hong Wan4, Ming-Ming Sun3
1Department of Emergency Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, China.
Insights
Cardamonin (CAR) protects against sepsis-induced heart dysfunction by reducing oxidative stress and apoptosis. This flavone targets Nrf2 and NF-κB pathways, offering a potential therapy for septic cardiomyopathy.
Area of Science:
- Cardiovascular Biology
- Pharmacology
- Molecular Medicine
Background:
- Sepsis-induced cardiac dysfunction, or septic cardiomyopathy, is a critical complication of gram-negative bacterial infections.
- Lipopolysaccharide (LPS) is a key endotoxin triggering sepsis-related heart failure, yet effective targeted therapies are lacking.
- Oxidative stress and apoptosis are major contributors to LPS-induced myocardial injury.
Purpose of the Study:
- To evaluate the cardioprotective effects of cardamonin (CAR), a natural flavone, against LPS-induced cardiac dysfunction.
- To elucidate the underlying mechanisms, focusing on oxidative stress, apoptosis, and inflammatory pathways.
Main Methods:
- Adult mice were challenged with LPS and treated with CAR (20 mg/kg, p.o.).
- Cardiac function was assessed using echocardiography and biochemical assays.
- In vitro studies utilized isolated mouse cardiomyocytes exposed to LPS and CAR.
Main Results:
- LPS challenge significantly impaired cardiac contractility, increased apoptosis, and induced oxidative stress and inflammation.
- CAR administration markedly attenuated these LPS-induced detrimental effects.
- CAR's protective action involved modulation of Nrf2 and NF-κB signaling pathways, as confirmed by in vitro experiments.
Conclusions:
- Cardamonin demonstrates significant cardioprotective effects against LPS-induced cardiac dysfunction and apoptosis.
- The therapeutic benefits of CAR are mediated through the Nrf2 and NF-κB signaling pathways.
- Cardamonin represents a promising therapeutic candidate for managing septic cardiomyopathy.
Abstract:
In patients with sepsis, lipopolysaccharide (LPS) from the outer membrane of gram-negative bacteria triggers cardiac dysfunction and heart failure, but target therapy for septic cardiomyopathy remains unavailable. In this study we evaluated the beneficial effects of cardamonin (CAR), a flavone existing in Alpinia plant, on endotoxemia-induced cardiac dysfunction and the underlying mechanisms with focus on oxidative stress and apoptosis. Adult mice were exposed to LPS (4 mg/kg, i.p. for 6 h) prior to functional or biochemical assessments. CAR (20 mg/kg, p.o.) was administered to mice immediately prior to LPS challenge. We found that LPS challenge compromised cardiac contractile function, evidenced by compromised fractional shortening, peak shortening, maximal velocity of shortening/relengthening, enlarged LV end systolic diameter and prolonged relengthening in echocardiography, and induced apoptosis, overt oxidative stress (O2- production and reduced antioxidant defense) associated with inflammation, phosphorylation of NF-κB and cytosolic translocation of transcriptional factor Nrf2. These deteriorative effects were greatly attenuated or mitigated by CAR administration. However, H&E and Masson's trichrome staining analysis revealed that neither LPS challenge nor CAR administration significantly affected cardiomyocyte cross-sectional area and interstitial fibrosis. Mouse cardiomyocytes were treated with LPS (4 µg/mL) for 6 h in the absence or presence of CAR (10 μM) in vitro. We found that addition of CAR suppressed LPS-induced defect in cardiomyocyte shortening, which was nullified by the Nrf2 inhibitor ML-385 or the NF-κB activator prostratin. Taken together, our results suggest that CAR administration protects against LPS-induced cardiac contractile abnormality, oxidative stress, apoptosis, and inflammation through Nrf2- and NF-κB-dependent mechanism.
