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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.


Related in: MedlinePlus

Bar plots of (A) mean percentage of M1 macrophages and (B) mean fluorescence intensity of CD80+/CD86+ in each group. Data are expressed as the mean ± standard deviation. #P<0.01 vs. the control; *P<0.01 vs. the model. CD, cluster of differentiation; LPS, lipopolysaccharide; IFN, interferon.
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f4-mmr-14-02-1091: Bar plots of (A) mean percentage of M1 macrophages and (B) mean fluorescence intensity of CD80+/CD86+ in each group. Data are expressed as the mean ± standard deviation. #P<0.01 vs. the control; *P<0.01 vs. the model. CD, cluster of differentiation; LPS, lipopolysaccharide; IFN, interferon.

Mentions: A commonly accepted marker profile for M1 macrophages is CD80+/CD86+. Cells with CD80+ and CD86+ surface markers can be identified as M1 macrophage (24). The present study observed few cells with CD80+/CD86+ surface markers prior to LPS/IFN-γ stimulation, while large quantities of M1 macrophages with high fluorescence intensity of CD80+/CD86+ surface markers were detected following LPS/IFN-γ stimulation (Figs. 3 and 4). Following treatment with different concentrations of mangiferin, the percentage of M1 macrophages in each mangiferin-treated group was reduced to various degrees. However, there was a statistically significant decrease in M1 macrophage percentage and cell CD80+/CD86+ surface markers mean fluorescence intensity in the 100 and 200 µmol/l mangiferin groups (P<0.01). Furthermore, the decreases in the 100 µmol/l mangiferin group was lower than in the 200 µmol/l group, but there was no significant difference between the two groups (Figs. 3 and 4).


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)

Bar plots of (A) mean percentage of M1 macrophages and (B) mean fluorescence intensity of CD80+/CD86+ in each group. Data are expressed as the mean ± standard deviation. #P<0.01 vs. the control; *P<0.01 vs. the model. CD, cluster of differentiation; LPS, lipopolysaccharide; IFN, interferon.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

f4-mmr-14-02-1091: Bar plots of (A) mean percentage of M1 macrophages and (B) mean fluorescence intensity of CD80+/CD86+ in each group. Data are expressed as the mean ± standard deviation. #P<0.01 vs. the control; *P<0.01 vs. the model. CD, cluster of differentiation; LPS, lipopolysaccharide; IFN, interferon.
Mentions: A commonly accepted marker profile for M1 macrophages is CD80+/CD86+. Cells with CD80+ and CD86+ surface markers can be identified as M1 macrophage (24). The present study observed few cells with CD80+/CD86+ surface markers prior to LPS/IFN-γ stimulation, while large quantities of M1 macrophages with high fluorescence intensity of CD80+/CD86+ surface markers were detected following LPS/IFN-γ stimulation (Figs. 3 and 4). Following treatment with different concentrations of mangiferin, the percentage of M1 macrophages in each mangiferin-treated group was reduced to various degrees. However, there was a statistically significant decrease in M1 macrophage percentage and cell CD80+/CD86+ surface markers mean fluorescence intensity in the 100 and 200 µmol/l mangiferin groups (P<0.01). Furthermore, the decreases in the 100 µmol/l mangiferin group was lower than in the 200 µmol/l group, but there was no significant difference between the two groups (Figs. 3 and 4).

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