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穿心莲内酯对小鼠腹腔巨噬细胞源性泡沫细胞丝裂原活化蛋白激酶和核因子-κB 激活的影响。

Effects of andrographolide on the activation of mitogen activated protein kinases and nuclear factor-κB in mouse peritoneal macrophage-derived foam cells.

机构信息

Department of Emergency, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

出版信息

Chin J Integr Med. 2012 May;18(5):391-4. doi: 10.1007/s11655-011-0700-8. Epub 2011 Apr 26.

Abstract

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.

摘要

目的

观察穿心莲内酯对巨噬细胞泡沫细胞中丝裂原活化蛋白激酶(MAPK)的激活和核因子-κB(NF-κB)表达的影响。

方法

用氧化型低密度脂蛋白(ox-LDL)、ox-LDL+穿心莲内酯或无处理(对照)培养小鼠腹腔巨噬细胞。用 Western blot 检测 MAPK 分子(p38MAPK、JNK、ERK1/2)的磷酸化和 NF-κB p65 的表达。

结果

与对照组细胞相比,ox-LDL 或 ox-LDL+穿心莲内酯培养的细胞中磷酸化 p38 和 NF-κB p65 的表达增加(P<0.01),但与 ox-LDL 相比,ox-LDL+穿心莲内酯存在时明显减弱(P<0.05)。与对照组细胞相比,ox-LDL 或 ox-LDL+穿心莲内酯存在时磷酸化 JNK 增加(P<0.01),但 ox-LDL 与 ox-LDL+穿心莲内酯之间无显著差异(P>0.05)。与对照组细胞相比,ox-LDL 存在时磷酸化 ERK1/2 的表达增加(P<0.01),但 ox-LDL+穿心莲内酯培养的细胞与对照培养基之间无显著差异(P>0.05)。

结论

穿心莲内酯可抑制 ox-LDL 诱导的巨噬细胞泡沫细胞中 ERK1/2、p38MAPK 和 NF-κB 的激活,这可能是其预防动脉粥样硬化的机制之一。

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