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Mangiferin inhibits macrophage classical activation via downregulating interferon regulatory factor 5 expression.

Wei Z, Yan L, Chen Y, Bao C, Deng J, Deng J - Mol Med Rep (2016)

Bottom Line: Mangiferin is a natural polyphenol and the predominant effective component of Mangifera indica Linn. leaves.The results of the present study demonstrated that mangiferin significantly inhibits LPS/IFN‑γ stimulation‑induced classical activation of macrophages in vitro and markedly decreases proinflammatory cytokine release.In addition, cellular IRF5 expression was markedly downregulated.

View Article: PubMed Central - PubMed

Affiliation: Guangxi Scientific Experimental Center of Traditional Chinese Medicine, Guangxi University of Chinese Medicine, Nanning, Guangxi 530001, P.R. China.

ABSTRACT
Mangiferin is a natural polyphenol and the predominant effective component of Mangifera indica Linn. leaves. For hundreds of years, Mangifera indica Linn. leaf has been used as an ingredient in numerous traditional Chinese medicine preparations for the treatment of bronchitis. However, the pharmacological mechanism of mangiferin in the treatment of bronchitis remains to be elucidated. Macrophage classical activation is important role in the process of bronchial airway inflammation, and interferon regulatory factor 5 (IRF5) has been identified as a key regulatory factor for macrophage classical activation. The present study used the THP‑1 human monocyte cell line to investigate whether mangiferin inhibits macrophage classical activation via suppressing IRF5 expression in vitro. THP‑1 cells were differentiated to macrophages by phorbol 12‑myristate 13‑acetate. Macrophages were polarized to M1 macrophages following stimulation with lipopolysaccharide (LPS)/interferon‑γ (IFN‑γ). Flow cytometric analysis was conducted to detect the M1 macrophages. Reverse transcription‑quantitative polymerase chain reaction was used to investigate cellular IRF5 gene expression. Levels of proinflammatory cytokines and IRF5 were assessed following cell culture and cellular homogenization using enzyme‑linked immunosorbent assay. IRF5 protein and nuclei co‑localization was performed in macrophages with laser scanning confocal microscope immunofluorescence analysis. The results of the present study demonstrated that mangiferin significantly inhibits LPS/IFN‑γ stimulation‑induced classical activation of macrophages in vitro and markedly decreases proinflammatory cytokine release. In addition, cellular IRF5 expression was markedly downregulated. These results suggest that the inhibitory effect of mangiferin on classical activation of macrophages may be exerted via downregulation of cellular IRF5 expression levels.

No MeSH data available.


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Mangifera indica Linn. leaves, mangiferin powder and the chemical structure.
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f1-mmr-14-02-1091: Mangifera indica Linn. leaves, mangiferin powder and the chemical structure.

Mentions: Mangiferin, (1,3,6,7-tetrahydroxyxanthone-C2-β-D-gluco side) is a natural polyphenol (1), and the predominant effective component of Mangifera indica Linn. leaf (Fig. 1) (2–4). For hundreds of years, Mangifera indica Linn. leaves have been used in southern China as an ingredient in various traditional Chinese medicine preparations for the treatment of bronchitis. However, the underlying pharmacological mechanism of mangiferin in the treatment of bronchitis remains to be elucidated. Previous studies have demonstrated mangiferin exerts marked anti-inflammatory properties, and the pharmacological mechanism is associated with markedly decreased release of proinflammatory cytokines (5,6). Bronchial airway inflammation is recognized as a characteristic pathological change in bronchitis (7). Peripheral blood monocytes migrate into the bronchus and surrounding lung tissue by chemotaxis. Monocytes in the lung tissue differentiates into macrophage and polarizes to M1 macrophages when activated by lipo-polysaccharide (LPS) or interferon-γ (IFN-γ) (8,9). This process is defined as macrophage classical activation (10). M1 macrophages produce and release large quantities of proinflammatory cytokines, including tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6) and interleukin-8 (IL-8) (11,12). Proinflammatory cytokines are important in human infection and non-infection immunity, however, excessive proinflammatory cytokines may result in tissue and cell damage (13,14). Serious tissue and cell damage can lead to deteriorating physiological function that may be life-threatening. Thus, M1 macrophages are crucial for the pathological process of bronchitis development. It may be a potential biological target of a therapeutic agent used to treat airway inflammation treatment, as targeting it may appropriately regulate polarization to M1 macrophages (15). Previous studies demonstrate that IRF5 is critical in macro-phage polarization to M1 macrophages, as polarization can be inhibited by suppression of IRF5 expression in macrophages (16,17). It remains to be elucidated whether mangiferin inhibits macrophage polarization to M1 macrophages via suppressing IRF5 expression, and thus decreasing proinflammatory cytokines releasing.


Mangiferin inhibits macrophage classical activation via downregulating interferon regulatory factor 5 expression.

Wei Z, Yan L, Chen Y, Bao C, Deng J, Deng J - Mol Med Rep (2016)

Mangifera indica Linn. leaves, mangiferin powder and the chemical structure.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4940072&req=5

f1-mmr-14-02-1091: Mangifera indica Linn. leaves, mangiferin powder and the chemical structure.
Mentions: Mangiferin, (1,3,6,7-tetrahydroxyxanthone-C2-β-D-gluco side) is a natural polyphenol (1), and the predominant effective component of Mangifera indica Linn. leaf (Fig. 1) (2–4). For hundreds of years, Mangifera indica Linn. leaves have been used in southern China as an ingredient in various traditional Chinese medicine preparations for the treatment of bronchitis. However, the underlying pharmacological mechanism of mangiferin in the treatment of bronchitis remains to be elucidated. Previous studies have demonstrated mangiferin exerts marked anti-inflammatory properties, and the pharmacological mechanism is associated with markedly decreased release of proinflammatory cytokines (5,6). Bronchial airway inflammation is recognized as a characteristic pathological change in bronchitis (7). Peripheral blood monocytes migrate into the bronchus and surrounding lung tissue by chemotaxis. Monocytes in the lung tissue differentiates into macrophage and polarizes to M1 macrophages when activated by lipo-polysaccharide (LPS) or interferon-γ (IFN-γ) (8,9). This process is defined as macrophage classical activation (10). M1 macrophages produce and release large quantities of proinflammatory cytokines, including tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6) and interleukin-8 (IL-8) (11,12). Proinflammatory cytokines are important in human infection and non-infection immunity, however, excessive proinflammatory cytokines may result in tissue and cell damage (13,14). Serious tissue and cell damage can lead to deteriorating physiological function that may be life-threatening. Thus, M1 macrophages are crucial for the pathological process of bronchitis development. It may be a potential biological target of a therapeutic agent used to treat airway inflammation treatment, as targeting it may appropriately regulate polarization to M1 macrophages (15). Previous studies demonstrate that IRF5 is critical in macro-phage polarization to M1 macrophages, as polarization can be inhibited by suppression of IRF5 expression in macrophages (16,17). It remains to be elucidated whether mangiferin inhibits macrophage polarization to M1 macrophages via suppressing IRF5 expression, and thus decreasing proinflammatory cytokines releasing.

Bottom Line: Mangiferin is a natural polyphenol and the predominant effective component of Mangifera indica Linn. leaves.The results of the present study demonstrated that mangiferin significantly inhibits LPS/IFN‑γ stimulation‑induced classical activation of macrophages in vitro and markedly decreases proinflammatory cytokine release.In addition, cellular IRF5 expression was markedly downregulated.

View Article: PubMed Central - PubMed

Affiliation: Guangxi Scientific Experimental Center of Traditional Chinese Medicine, Guangxi University of Chinese Medicine, Nanning, Guangxi 530001, P.R. China.

ABSTRACT
Mangiferin is a natural polyphenol and the predominant effective component of Mangifera indica Linn. leaves. For hundreds of years, Mangifera indica Linn. leaf has been used as an ingredient in numerous traditional Chinese medicine preparations for the treatment of bronchitis. However, the pharmacological mechanism of mangiferin in the treatment of bronchitis remains to be elucidated. Macrophage classical activation is important role in the process of bronchial airway inflammation, and interferon regulatory factor 5 (IRF5) has been identified as a key regulatory factor for macrophage classical activation. The present study used the THP‑1 human monocyte cell line to investigate whether mangiferin inhibits macrophage classical activation via suppressing IRF5 expression in vitro. THP‑1 cells were differentiated to macrophages by phorbol 12‑myristate 13‑acetate. Macrophages were polarized to M1 macrophages following stimulation with lipopolysaccharide (LPS)/interferon‑γ (IFN‑γ). Flow cytometric analysis was conducted to detect the M1 macrophages. Reverse transcription‑quantitative polymerase chain reaction was used to investigate cellular IRF5 gene expression. Levels of proinflammatory cytokines and IRF5 were assessed following cell culture and cellular homogenization using enzyme‑linked immunosorbent assay. IRF5 protein and nuclei co‑localization was performed in macrophages with laser scanning confocal microscope immunofluorescence analysis. The results of the present study demonstrated that mangiferin significantly inhibits LPS/IFN‑γ stimulation‑induced classical activation of macrophages in vitro and markedly decreases proinflammatory cytokine release. In addition, cellular IRF5 expression was markedly downregulated. These results suggest that the inhibitory effect of mangiferin on classical activation of macrophages may be exerted via downregulation of cellular IRF5 expression levels.

No MeSH data available.


Related in: MedlinePlus