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Published on: December 26, 2017
Effects of andrographolide on the activation of mitogen activated protein kinases and nuclear factor-κB in mouse
1Department of Emergency, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Objective:
To observe the effect of andrographolide on the activation of mitogen-activated protein kinases (MAPKs) and expression of nuclear factor-κB (NF-κB) in macrophage foam cells.
Methods:
The mouse peritoneal macrophages were cultured in the media in the presence of oxidized low-density lipoprotein (ox-LDL), ox-LDL+andrographolide, or neither (control). The phosphorylation of MAPK molecules (p38MAPK, JNK, ERK1/2) and the expressions of NK-κB p65 were examined by Western blot.
Results:
As compared with cells in the control group, the expressions of phospho-p38 and NF-κB p65 were increased in the cells cultured with either ox-LDL or ox-LDL+andrographolide (P<0.01), but attenuated significantly in the presence of ox-LDL+ andrographolide when compared with ox-LDL (P<0.05). The phospho-JNK increased in the presence of either ox-LDL or ox-LDL+andrographolide when compared with control cells (P<0.01), but no significant difference existed between ox-LDL and ox-LDL+andrographolide (P>0.05). The expression of phospho-ERK1/2 was increased in the presence of ox-LDL compared with the control cells (P<0.01), but no significant differences existed between the cells cultured in the presence of ox-LDL+andrographolide and the control medium (P>0.05).
Conclusions:
Andrographolide could inhibit the activation of ERK1/2, p38MAPK and NK-κB induced by ox-LDL in macrophage foam cells, which might be one of its mechanisms in preventing atherosclerosis.
Insights
Andrographolide inhibits key inflammatory pathways in macrophage foam cells. This compound may offer a mechanism for preventing atherosclerosis by reducing ox-LDL-induced activation of NF-κB and MAPKs.
Area of Science:
- Cell Biology
- Immunology
- Pharmacology
Background:
- Macrophage foam cells are central to atherosclerosis development.
- Oxidized low-density lipoprotein (ox-LDL) promotes inflammation in macrophages.
- Mitogen-activated protein kinases (MAPKs) and nuclear factor-κB (NF-κB) are critical inflammatory mediators.
Purpose of the Study:
- To investigate the effect of andrographolide on MAPK and NF-κB activation in macrophage foam cells.
- To determine if andrographolide modulates ox-LDL-induced inflammatory responses.
- To explore potential anti-atherosclerotic mechanisms of andrographolide.
Main Methods:
- Mouse peritoneal macrophages were treated with ox-LDL and/or andrographolide.
- Western blot analysis was used to detect phosphorylated MAPKs (p38MAPK, JNK, ERK1/2).
- NF-κB p65 expression was quantified using Western blot.
Main Results:
- Ox-LDL increased the expression of phospho-p38 and NF-κB p65.
- Andrographolide significantly attenuated the ox-LDL-induced increase in phospho-p38 and NF-κB p65.
- Ox-LDL increased phospho-JNK and phospho-ERK1/2; andrographolide inhibited phospho-ERK1/2 but not phospho-JNK compared to ox-LDL alone.
Conclusions:
- Andrographolide inhibits ox-LDL-induced activation of ERK1/2, p38MAPK, and NF-κB in macrophage foam cells.
- These inhibitory effects suggest a role for andrographolide in preventing atherosclerosis.
- Andrographolide's modulation of inflammatory signaling pathways is a potential therapeutic mechanism.
