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Updated: Jun 26, 2025
Isolation, Characterization, and Purification of Macrophages from Tissues Affected by Obesity-related Inflammation
Published on: April 3, 2017
Naringin Inhibits Macrophage Foam Cell Formation by Regulating Lipid Homeostasis and Metabolic Phenotype
Yan Liu1,2, Xiaohan Tang1, Hailong Yuan1
1Department of Pharmacy, Air Force Medical Center, PLA, Beijing 100142, China.
Abstract:
Imbalances in lipid uptake and efflux and inflammation are major contributors to foam cell formation, which is considered a therapeutic target to protect against atherosclerosis. Naringin, a citrus flavonoid abundant in citrus fruits, has been reported to exert an antiatherogenic function, but its pharmacological mechanism is unclear. Naringin treatment effectively inhibits foam cell formation in THP-1 and RAW264.7 macrophages. In this study, mechanically, naringin maintained lipid homeostasis within macrophages through downregulation of the key genes for lipid uptake (MSR1 and CD36) and the upregulation of ABCA1, ABCG1 and SR-B1, which are responsible for cholesterol efflux. Meanwhile, naringin significantly decreased the cholesterol synthesis-related genes and increased the genes involved in cholesterol metabolism. Subsequently, the results showed that ox-LDL-induced macrophage inflammatory responses were inhibited by naringin by reducing the proinflammatory cytokines IL-1β, IL-6 and TNF-α, and increasing the anti- inflammatory cytokine IL-10, which was further verified by the downregulation of pro-inflammatory and chemokine-related genes. Additionally, we found that naringin reprogrammed the metabolic phenotypes of macrophages by suppressing glycolysis and promoting lipid oxidation metabolism to restore macrophage phenotypes and functions. These results suggest that naringin is a potential drug for the treatment of AS as it inhibits macrophage foam cell formation by regulating metabolic phenotypes and inflammation.
Insights
Naringin, a citrus flavonoid, inhibits foam cell formation in macrophages by regulating lipid metabolism and inflammation. This suggests naringin is a potential therapeutic agent for atherosclerosis treatment.
Area of Science:
- Biochemistry
- Molecular Biology
- Pharmacology
Background:
- Foam cell formation, driven by lipid imbalance and inflammation, is a key factor in atherosclerosis.
- Naringin, a citrus flavonoid, shows antiatherogenic potential, but its mechanism remains unclear.
Purpose of the Study:
- To elucidate the pharmacological mechanism of naringin in inhibiting foam cell formation.
- To investigate naringin's effects on lipid metabolism, inflammation, and metabolic phenotypes in macrophages.
Main Methods:
- Naringin treatment of THP-1 and RAW264.7 macrophages.
- Gene expression analysis of lipid uptake/efflux, cholesterol synthesis/metabolism, and inflammatory markers.
- Assessment of inflammatory cytokines and metabolic reprogramming (glycolysis and lipid oxidation).
Main Results:
- Naringin inhibited foam cell formation by regulating lipid homeostasis genes (downregulating uptake genes like MSR1/CD36, upregulating efflux genes like ABCA1/ABCG1/SR-B1).
- Naringin reduced pro-inflammatory cytokines (IL-1β, IL-6, TNF-α) and increased anti-inflammatory IL-10.
- Naringin suppressed glycolysis and promoted lipid oxidation, reprogramming macrophage metabolic phenotypes.
Conclusions:
- Naringin effectively inhibits macrophage foam cell formation by modulating lipid metabolism and inflammatory responses.
- Naringin's ability to reprogram macrophage metabolic phenotypes suggests its potential as a therapeutic agent for atherosclerosis (AS).
