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蒲公英甾醇对脂多糖诱导的RAW 264.7巨噬细胞中诱导型一氧化氮合酶和环氧化酶-2表达的影响。

Effects of taraxasterol on iNOS and COX-2 expression in LPS-induced RAW 264.7 macrophages.

作者信息

Xiong Huanzhang, Cheng Yao, Zhang Xian, Zhang Xuemei

机构信息

Department of Animal Medicine, Agricultural College of Yanbian University, Gongyuan Street, Yanji, Jilin 133002, PR China.

Department of Animal Medicine, Agricultural College of Yanbian University, Gongyuan Street, Yanji, Jilin 133002, PR China.

出版信息

J Ethnopharmacol. 2014 Aug 8;155(1):753-7. doi: 10.1016/j.jep.2014.06.023. Epub 2014 Jun 16.

Abstract

ETHNOPHARMACOLOGICAL RELEVANCE

Taraxasterol was isolated from the Chinese medicinal herb Taraxacum officinale which has been frequently used as a remedy for inflammatory diseases. Our previous study has shown that taraxasterol inhibited lipopolysaccharide (LPS)-induced nitric oxide (NO) and prostaglandin E2 (PGE2) production in RAW 264.7 macrophages. To elucidate the underlying mechanism responsible for these effects, in the present study, we investigated the effects of taraxasterol on inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) expression, and mitogen-activated protein kinases (MAPKs) signaling pathway in LPS-induced RAW 264.7 macrophages.

MATERIALS AND METHODS

RAW 264.7 cells were pretreated with 2.5, 5 and 12.5 μg/ml of taraxasterol 1 h prior to treatment with 1 μg/ml of LPS. The mRNA expression levels of iNOS and COX-2 were examined by RT-PCR. The protein expression levels of iNOS and COX-2, and the phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2), p38 and c-Jun N-terminal kinase (JNK) MAPKs were measured by Western blot.

RESULTS

The mRNA and protein expression levels of iNOS and COX-2 were inhibited by taraxasterol in a concentration-dependent manner. Further studies revealed that taraxasterol suppressed the phosphorylation of ERK1/2 and p38 in LPS-induced RAW 264.7 macrophages.

CONCLUSIONS

These results indicate that taraxasterol inhibits iNOS and COX-2 expression by blocking ERK1/2 and p38 MAPKs signaling pathway.

摘要

民族药理学相关性

蒲公英甾醇是从中国药用植物蒲公英中分离得到的,蒲公英常被用作治疗炎症性疾病的药物。我们之前的研究表明,蒲公英甾醇可抑制脂多糖(LPS)诱导的RAW 264.7巨噬细胞中一氧化氮(NO)和前列腺素E2(PGE2)的产生。为了阐明这些作用的潜在机制,在本研究中,我们研究了蒲公英甾醇对LPS诱导的RAW 264.7巨噬细胞中诱导型一氧化氮合酶(iNOS)和环氧化酶-2(COX-2)表达以及丝裂原活化蛋白激酶(MAPKs)信号通路的影响。

材料与方法

RAW 264.7细胞在用1μg/ml LPS处理前1小时,分别用2.5、5和12.5μg/ml的蒲公英甾醇进行预处理。通过RT-PCR检测iNOS和COX-2的mRNA表达水平。通过蛋白质印迹法检测iNOS和COX-2的蛋白质表达水平以及细胞外信号调节激酶1/2(ERK1/2)、p38和c-Jun氨基末端激酶(JNK)MAPKs的磷酸化水平。

结果

蒲公英甾醇以浓度依赖性方式抑制iNOS和COX-2的mRNA和蛋白质表达水平。进一步研究表明,蒲公英甾醇抑制LPS诱导的RAW 264.7巨噬细胞中ERK1/2和p38的磷酸化。

结论

这些结果表明,蒲公英甾醇通过阻断ERK1/2和p38 MAPKs信号通路抑制iNOS和COX-2的表达。

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