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Published on: September 12, 2019
Silymarin Inhibits Morphological Changes in LPS-Stimulated Macrophages by Blocking NF-κB Pathway
Eun Jeong Kim1, Min Young Lee1, Young Jin Jeon1
1Department of Pharmacology, School of Medicine, Chosun University, Gwangju 501-759, Korea.
Abstract:
The present study showed that silymarin, a polyphenolic flavonoid isolated from milk thistle (Silybum marianum), inhibited lipopolysaccharide (LPS)-induced morphological changes in the mouse RAW264.7 macrophage cell line. We also showed that silymarin inhibited the nuclear translocation and transactivation activities of nuclear factor-kappa B (NF-κB), which is important for macrophage activation-associated changes in cell morphology and gene expression of inflammatory cytokines. BAY-11-7085, an NF-κB inhibitor, abrogated LPS-induced morphological changes and NO production, similar to silymarin. Treatment of RAW264.7 cells with silymarin also inhibited LPS-stimulated activation of mitogen-activated protein kinases (MAPKs). Collectively, these experiments demonstrated that silymarin inhibited LPS-induced morphological changes in the RAW264.7 mouse macrophage cell line. Our findings indicated that the most likely mechanism underlying this biological effect involved inhibition of the MAPK pathway and NF-κB activity. Inhibition of these activities by silymarin is a potentially useful strategy for the treatment of inflammation because of the critical roles played by MAPK and NF-κB in mediating inflammatory responses in macrophages.
Insights
Silymarin, derived from milk thistle, prevents inflammatory changes in macrophage cells by inhibiting key pathways. This natural compound offers a potential strategy for treating inflammation.
Area of Science:
- Immunology
- Pharmacology
- Cell Biology
Background:
- Macrophage activation by lipopolysaccharide (LPS) leads to morphological changes and inflammatory cytokine production.
- Nuclear factor-kappa B (NF-κB) and mitogen-activated protein kinases (MAPKs) are critical signaling pathways in macrophage activation.
Purpose of the Study:
- To investigate the effect of silymarin on LPS-induced changes in RAW264.7 macrophage cells.
- To elucidate the molecular mechanisms underlying silymarin's anti-inflammatory effects.
Main Methods:
- RAW264.7 macrophage cell line treated with LPS and silymarin.
- Analysis of NF-κB translocation and transactivation.
- Assessment of MAPK pathway activation.
- Measurement of nitric oxide (NO) production.
Main Results:
- Silymarin inhibited LPS-induced morphological changes in RAW264.7 cells.
- Silymarin suppressed NF-κB nuclear translocation and transactivation.
- Silymarin treatment reduced LPS-stimulated MAPK activation.
- BAY-11-7085, an NF-κB inhibitor, mimicked silymarin's effects on morphology and NO production.
Conclusions:
- Silymarin effectively inhibits LPS-induced macrophage activation.
- The anti-inflammatory mechanism of silymarin involves the inhibition of both NF-κB and MAPK signaling pathways.
- Silymarin represents a promising therapeutic agent for inflammatory conditions due to its modulation of macrophage inflammatory responses.

