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槐角通过调节脂多糖刺激的RAW 264.7巨噬细胞中的NF-κB和MAPK信号通路,减弱促炎介质和细胞因子的分泌。

Fructus sophorae attenuates secretion of proinflammatory mediators and cytokines through the modulation of NF-κB and MAPK signaling pathways in LPS-stimulated RAW 264.7 macrophages.

作者信息

Choi Yung Hyun, Kang Hye-Joo

机构信息

Department of Biochemistry, Dongeui University College of Korean Medicine, 52-57, Yangjeong-ro, Busanjin, Busan 614-052, Republic of Korea.

出版信息

Gen Physiol Biophys. 2016 Jul;35(3):323-31. doi: 10.4149/gpb_2015043. Epub 2016 Apr 5.

DOI:10.4149/gpb_2015043
PMID:27045671
Abstract

This study investigated the inhibitory effects and underlying mechanisms of fructus sophorae, the dried ripe fruit of Styphnolobium japonicum (L.) Schott, on the production of proinflammatory molecules in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages. The results indicated that pretreatment with noncytotoxic concentrations of fructus sophorae extract (FSE) significantly inhibited the release of the proinflammatory mediators nitric oxide (NO) and prostaglandin E(2), which were associated with the downregulation of both mRNA and protein for inducible NO synthase and cyclooxygenase-2, respectively, in LPS-challenged RAW 264.7 cells. FSE also blocked the LPS-induced expression of the proinflammatory cytokines interleukin (IL)-6 and IL-1β. Furthermore, the results showed that FSE efficiently attenuated the LPS-induced nuclear translocation of nuclear factor-kappa B (NF-κB) and phosphorylation of the mitogen-activated protein kinases (MAPKs) extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK) but not p38 MAPK. These results suggest that FSE exhibits anti-inflammatory activity by inhibiting proinflammatory mediators and cytokines through the inactivation of NF-κB, ERK and JNK, and it may offer therapeutic potential for treating inflammatory diseases accompanied with macrophage activation.

摘要

本研究调查了槐树(槐属植物日本槐的干燥成熟果实)对脂多糖(LPS)刺激的RAW 264.7巨噬细胞中促炎分子产生的抑制作用及其潜在机制。结果表明,用无细胞毒性浓度的槐果提取物(FSE)预处理可显著抑制促炎介质一氧化氮(NO)和前列腺素E2的释放,这分别与LPS刺激的RAW 264.7细胞中诱导型NO合酶和环氧化酶-2的mRNA和蛋白下调有关。FSE还阻断了LPS诱导的促炎细胞因子白细胞介素(IL)-6和IL-1β的表达。此外,结果表明,FSE有效减弱了LPS诱导的核因子κB(NF-κB)的核转位以及丝裂原活化蛋白激酶(MAPK)细胞外信号调节激酶(ERK)和c-Jun氨基末端激酶(JNK)的磷酸化,但对p38 MAPK无影响。这些结果表明,FSE通过使NF-κB、ERK和JNK失活来抑制促炎介质和细胞因子,从而表现出抗炎活性,并且它可能为治疗伴有巨噬细胞活化的炎症性疾病提供治疗潜力。

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