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寄生在甜槠树上的绒毛钩藤提取物对 LPS 刺激的 RAW264.7 细胞的抗炎作用。

Anti-inflammatory effect of the extracts from the branch of Taxillus yadoriki being parasitic in Neolitsea sericea in LPS-stimulated RAW264.7 cells.

机构信息

Department of Medicinal Plant Resources, Andong National University, Andong 36729, Republic of Korea.

Forest Medicinal Resources Research Center, National Institute of Forest Science, Yeongju 36040, Republic of Korea.

出版信息

Biomed Pharmacother. 2018 Aug;104:1-7. doi: 10.1016/j.biopha.2018.05.034. Epub 2018 May 11.

Abstract

Mistletoe has been used as the herbal medicine to treat hypertension, diabetes mellitus, inflammation, arthritis and viral infection. In this study, we evaluated the anti-inflammatory effect of extracts of branch from Taxillus yadoriki being parasitic in Neolitsea sericea (TY-NS-B) using in vitro model. TY-NS-B significantly inhibited LPS-induced secretion of NO and PGE in RAW264.7 cells. TY-NS-B was also observed to inhibit LPS-mediated iNOS COX-2 expression. In addition, TY-NS-B attenuated production of inflammatory cytokines such as TNF-α and IL-1β induced by LPS. TY-NS-B blocked LPS-mediated inhibitor of IκB-α, and inhibited p65 translocation to the nucleus and NF-κB activation. Furthermore, TY-NS-B reduced the phosphorylation of MAPKs such as p38 and JNK, but not ERK1/2. In addition, TY-NS-B increased ATF3 expression and ATF3 knockdown by ATF3 siRNA attenuated TY-NS-B-mediated inhibition of pro-inflammatory mediator expression. Collectively, our results suggest that TY-NS-B exerts potential anti-inflammatory effects by suppressing NF-κB and MAPK signaling activation, and increasing ATF3 expression. These findings indicate that TY-NS-B could be further developed as an anti-inflammatory drug.

摘要

槲寄生被用作草药来治疗高血压、糖尿病、炎症、关节炎和病毒感染。在这项研究中,我们使用体外模型评估了寄生于甜柿 Neolitsea sericea 上的 Taxillus yadoriki 枝条提取物(TY-NS-B)的抗炎作用。TY-NS-B 显著抑制了 LPS 诱导的 RAW264.7 细胞中 NO 和 PGE 的分泌。TY-NS-B 还观察到抑制 LPS 介导的 iNOS 和 COX-2 表达。此外,TY-NS-B 减弱了 LPS 诱导的 TNF-α和 IL-1β等炎症细胞因子的产生。TY-NS-B 阻断了 LPS 介导的 IκB-α抑制剂,抑制了 p65 向核内的易位和 NF-κB 的激活。此外,TY-NS-B 减少了 MAPKs 如 p38 和 JNK 的磷酸化,但不影响 ERK1/2。此外,TY-NS-B 增加了 ATF3 的表达,而 ATF3 siRNA 敲低 ATF3 则减弱了 TY-NS-B 介导的促炎介质表达的抑制作用。综上所述,我们的结果表明,TY-NS-B 通过抑制 NF-κB 和 MAPK 信号通路的激活以及增加 ATF3 的表达来发挥潜在的抗炎作用。这些发现表明,TY-NS-B 可以进一步开发为一种抗炎药物。

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