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槲皮素通过丝裂原活化蛋白激酶和核因子κB信号通路抑制脂多糖刺激的巨噬细胞中促炎细胞因子的产生。

Quercetin suppresses proinflammatory cytokines production through MAP kinases andNF-kappaB pathway in lipopolysaccharide-stimulated macrophage.

作者信息

Cho Sung-Yeon, Park Sang-Joon, Kwon Myung-Ja, Jeong Tae-Sook, Bok Song-Hae, Choi Woo-Young, Jeong Won-Il, Ryu Si-Yun, Do Sun-Hee, Lee Cha-Soo, Song Jae-Chan, Jeong Kyu-Shik

机构信息

Korea Research Institute of Bioscience and Biotechnology, Yusung, Taejon City, South Korea.

出版信息

Mol Cell Biochem. 2003 Jan;243(1-2):153-60. doi: 10.1023/a:1021624520740.

DOI:10.1023/a:1021624520740
PMID:12619901
Abstract

Quercetin is a flavonoid molecule ubiquitous in nature and functions as an anti-oxidant and anti-inflammatory agent with little toxicity in vivo and in vitro. Dose- and time-dependent effect of quercetin has been investigated on proinflammatory cytokine expression and NO production, focusing on its effects on the MAP kinases and the NF-kappaB signal transduction pathways in LPS-stimulated RAW 264.7 cells by using RT-PCR and immunoblotting. Quercetin strongly reduced activation of phosphorylated ERK kinase and p38 MAP kinase but not JNK MAP kinase by LPS treatment. In addition, quercetin treatment inhibited NF-kappaB activation through stabilization of the NF-kappaB/IkappaB complex and IkappaB degradation and proinflammatory cytokines and NO/iNOS expression. Quercetin may exert its anti-inflammatory and immunomodulatory properties in the effect molecules such as proinflammatory cytokines and NO/iNOS by suppressing the activation of ERK and p38 MAP kinase, and NF-kappaB/IkappaB signal transduction pathways.

摘要

槲皮素是一种在自然界中普遍存在的类黄酮分子,具有抗氧化和抗炎作用,在体内和体外的毒性都很小。通过逆转录聚合酶链反应(RT-PCR)和免疫印迹法,研究了槲皮素对促炎细胞因子表达和一氧化氮(NO)生成的剂量和时间依赖性影响,重点关注其对脂多糖(LPS)刺激的RAW 264.7细胞中丝裂原活化蛋白激酶(MAP激酶)和核因子κB(NF-κB)信号转导途径的影响。通过LPS处理,槲皮素强烈降低了磷酸化细胞外信号调节激酶(ERK激酶)和p38 MAP激酶的激活,但对c-Jun氨基末端激酶(JNK MAP激酶)没有影响。此外,槲皮素处理通过稳定NF-κB/IκB复合物、抑制IκB降解以及促炎细胞因子和NO/诱导型一氧化氮合酶(iNOS)的表达,抑制了NF-κB的激活。槲皮素可能通过抑制ERK和p38 MAP激酶以及NF-κB/IκB信号转导途径的激活,在促炎细胞因子和NO/iNOS等效应分子中发挥其抗炎和免疫调节特性。

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