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Updated: Nov 25, 2025
Preparation of Naringenin Solution for In Vivo Application
Published on: August 10, 2021
Mechanism of Naringenin Blocking the Protection of LTB4/BLT1 Receptor Against Septic Cardiac Dysfunction
Gang Ye1, Minna Wang2, Delin Liu2
1Department of Emergency Intensive Care Unit, Beijing LuHe Hospital, Capital Medical University, Beijing, China gangye231@aliyun.com.
Objective:
To investigate the possible role of Naringenin in AMPK signaling pathway in LPS-induced septic cardiac dysfunction in mice and to elucidate the inherent mechanism.
Methods:
Male C57 mice were used in the establishment of mouse sepsis model. The effect of Naringenin on septic cardiac dysfunction was observed. Echocardiographic parameters were recorded. Western blot was employed to detect the expressions of BCL-2, BAX, cleaved caspase-3, pNF-kB and IkB-α. Myocardial mitochondria were isolated and extracted. Real-time PCR was applied to detect the expressions of Cox4i, Cox5a mRNA, mt-Nd1, mt-Nd2, mt-Co1 and mt-Co2 mRNA. Western blot was employed to detect the expressions of Complex I, Complex II, and OPA1 to evaluate the effects of Naringenin on myocardial mitochondrial biology and function in septic cardiac dysfunction.
Results:
The expressions of TNF-α, IL-6, pNF-κB and IκB-α have changed after Naringenin treatment. IκB-α expression was decreased, expressions of TNF-α, IL-6 and pNF-κB were increased. Naringenin has significantly inhibited AMPK and ACC phosphorylation, and decreased PGC1α expression. Moreover, Naringenin reversed the increased expressions of PGC1α and phosphorylation of AMPK and ACC by U75302 treatment, and decreased the expressions of complex I, complex II and OPA1.
Conclusion:
Naringenin inhibits LTB4/BLT1 receptors to attenuate cardiomyocyte inflammation and apoptosis, which may mediate the protective effect of anti-septic cardiac dysfunction by activating AMPK signaling pathway and inhibiting NF-κB signaling and mitochondrial damage.
Insights
Naringenin protects against septic cardiac dysfunction by activating the AMPK pathway and inhibiting inflammation and mitochondrial damage. This study elucidates its protective mechanism in a mouse model.
Area of Science:
- Biochemistry
- Cardiology
- Pharmacology
Background:
- Sepsis-induced cardiac dysfunction is a critical complication.
- Naringenin's therapeutic potential requires mechanistic elucidation.
- The role of the AMPK signaling pathway in sepsis is under investigation.
Purpose of the Study:
- To investigate Naringenin's role in the AMPK signaling pathway in LPS-induced septic cardiac dysfunction.
- To elucidate the underlying mechanism of Naringenin's protective effects.
Main Methods:
- Established a mouse sepsis model using LPS.
- Administered Naringenin and assessed cardiac function via echocardiography.
- Utilized Western blot and real-time PCR to analyze key protein and mRNA expressions, including apoptotic markers, NF-κB pathway components, and mitochondrial proteins.
Main Results:
- Naringenin modulated TNF-α, IL-6, pNF-κB, and IκB-α expressions.
- Naringenin inhibited AMPK and ACC phosphorylation and decreased PGC1α expression.
- Naringenin reversed U75302-induced changes and reduced mitochondrial complex I, II, and OPA1 expressions.
Conclusions:
- Naringenin attenuates cardiomyocyte inflammation and apoptosis.
- Naringenin activates the AMPK signaling pathway.
- Naringenin inhibits NF-κB signaling and mitigates mitochondrial damage, conferring protection against septic cardiac dysfunction.
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