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Kaempferitrin Attenuates Lipopolysaccharide-Induced Cardiac Dysfunction Through Suppression of the NF-κB/NLRP3
Hongyu Kuang1, Qiang Li2, Min Chen3
1Department of Cardiology, University-Town Hospital of Chongqing Medical University, Chongqing, China.
Insights
Kaempferitrin (Kae) protects against sepsis-induced heart dysfunction by inhibiting the NF-κB/NLRP3 inflammatory pathway. This flavonoid compound reduces cardiomyocyte injury and apoptosis, offering a potential therapeutic strategy for septic cardiomyopathy.
Area of Science:
- Cardiovascular Research
- Molecular Biology
- Pharmacology
Background:
- Sepsis-induced cardiac dysfunction involves cardiomyocyte inflammation and metabolic disorders.
- Kaempferitrin (Kae), a flavonoid, exhibits anti-inflammatory and anti-glycation properties.
- Investigating Kae's protective effects against sepsis-induced cardiac dysfunction is crucial.
Purpose of the Study:
- To evaluate the protective effects of Kaempferitrin (Kae) against lipopolysaccharide (LPS)-induced cardiac dysfunction in a mouse model.
- To elucidate the underlying molecular mechanisms, focusing on the NF-κB/NLRP3 signaling pathway.
Main Methods:
- In vivo studies involved treating C57BL/6J mice with Kae followed by LPS, with subsequent echocardiography, serum tests, and pathological analysis.
- Transcriptomics, western blotting, and RT-PCR were employed to explore molecular mechanisms.
- In vitro experiments utilized H9c2 and AC16 cardiomyocyte cell lines pretreated with Kae and stimulated with LPS.
Main Results:
- Kae pretreatment mitigated LPS-induced cardiac dysfunction, reducing pro-inflammatory cytokines (IL-6, TNF-α, IL-1β, IL-18) and cardiomyocyte injury/apoptosis.
- Transcriptomic analysis identified the NF-κB/NLRP3 signaling pathway as a key mechanism, showing Kae attenuated LPS-induced activation and pyroptosis.
- In vitro and NLRP3-knockout mouse models confirmed Kae's inhibition of the NF-κB/NLRP3 pathway and its protective role in septic cardiomyopathy.
Conclusions:
- Kaempferitrin (Kae) alleviates left ventricular remodeling and cardiac dysfunction in sepsis.
- The protective mechanism involves the suppression of the NF-κB/NLRP3/pyroptosis pathway.
- Kae demonstrates potential as a therapeutic agent for sepsis-related cardiac complications.
Purpose:
The inflammatory activation and metabolic disorders of cardiomyocytes are essential mechanisms in sepsis-related cardiac dysfunction. Kaempferitrin (Kae), a flavonoid compound, possesses various properties including anti-inflammatory and anti-glycation effects. Hence, the current study is conducted to investigate the protective effects of Kae against sepsis-induced cardiac dysfunction.
Methods:
C57BL/6 J mice were treated with Kae for 2 h, followed by lipopolysaccharide (LPS) treatment. After 12 h, the echocardiographic measurements were conducted. Serum test, pathological analysis, transcriptomics, western blotting, and RT-PCR were used for exploring mechanisms. Additionally, in vitro, H9c2 and AC16 cardiomyocyte cell lines were pretreated with Kae (10 μM) for 2 h, followed by LPS stimulation (1 μg/mL).
Results:
In vivo, pretreatment with Kae mitigates LPS-induced cardiac dysfunction. Kae suppresses the levels of IL-6, TNF-α, IL-1β, and IL-18 in the cardiac tissue of mice mediated by LPS. Additionally, serological and histological assessments demonstrate that Kae exhibits protective effects against LPS-induced cardiomyocyte injury and apoptosis. Transcriptomic analysis reveals that the nuclear factor kappa-B (NF-κB)/NLRP3 signaling pathway may be a crucial mechanism. Meanwhile, it proved that LPS significantly activates NF-κB/NLRP3 to induce cardiomyocyte pyroptosis, which is attenuated by Kae. In vitro, H9c2 and AC16 cardiomyocyte cell lines were pretreated with Kae followed by LPS stimulation, showing an inhibition of NF-κB/NLRP3 pathway, with a decreased mRNA levels of Il-6, Tnf-α, Il-1β. The NLRP3-knock out (Nlrp3 -/- ) mice have verified that Kae ameliorating LPS-induced spetic cardiomyopathy by inhibiting NLRP3.
Conclusions:
This study confirms that Kae alleviates LPS-induced left ventricular remodeling and cardiac dysfunction by suppressing the NF-κB/NLRP3/pyroptosis pathway.
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