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Effects of Andrographolide on the Activation of Mitogen Activated Protein Kinases and Nuclear Factor-κ B in Mouse Peritoneal Macrophage-derived Foam Cells 被引量:6
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作者 李福星 李树生 《Chinese Journal of Integrative Medicine》 SCIE CAS 2012年第5期391-394,共4页
Objective: To observe the effect of andrographolide on the activation of mitogen-activated protein kinases (MAPKs) and expression of nuclear factor- kB (NF-kB) in macrophage foam cells. Methods: The mouse perito... Objective: To observe the effect of andrographolide on the activation of mitogen-activated protein kinases (MAPKs) and expression of nuclear factor- kB (NF-kB) 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- kB p65 were examined by Western blot. Results: As compared with cells in the control group, the expressions of phospho-p38 and NF- kB 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-kB induced by ox-LDL in macrophage foam cells, which might be one of its mechanisms in preventing atherosclerosis. 展开更多
关键词 ANDROGRAPHOLIDE mouse peritoneal macrophage foam cells mitogen activated protein kinasese nuclear factor-kB ATHEROSCLEROSIS
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