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竹沥抑制人角质形成细胞中胸腺和激活调节趋化因子及巨噬细胞衍生趋化因子的表达与其抗氧化作用有关。

Bambusae caulis in Liquamen Suppresses the Expression of Thymus and Activation-Regulated Chemokine and Macrophage-Derived Chemokine in Human Keratinocytes due to Antioxidant Effect.

机构信息

Key Laboratory for Regenerative Medicine, Ministry of Education, Jinan University, Guangzhou 510632, China.

出版信息

Evid Based Complement Alternat Med. 2012;2012:617494. doi: 10.1155/2012/617494. Epub 2011 Jul 6.

DOI:10.1155/2012/617494
PMID:21785648
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3137989/
Abstract

Bambusae caulis in Liquamen (BCL), traditional herbal medicine used in East Asia, is known to have antioxidative and immune-regulating properties. We hypothesized that the potential antioxidant effects of BCL might suppress the production of thymus and activation-regulated chemokine (TARC) and macrophage-derived chemokine (MDC) in human keratinocytes (HaCaT cell). The immune-regulating effect of BCL was demonstrated by antioxidant capacity using DPPH analysis and DCFH-DA analysis. We found that BCL had strong ROS scavenge effect in HaCaT cell. BCL also showed suppression of IFN-γ-induced expression of TARC and MDC, activation of NF-κB, and, moreover, significant block of IFN-γ-induced degradation and phosphorylation of IκB. However, it had no effects on phosphorylation of p38 MAPK. Collectively, these results suggest that BCL may have a therapeutic potential on skin disease such as atopic dermatitis by inhibiting Th2 chemokines which is due, at least in part, to its antioxidant capacities.

摘要

竹液(BCL),一种传统的东亚草药,已知具有抗氧化和免疫调节特性。我们假设 BCL 的潜在抗氧化作用可能会抑制人角质形成细胞(HaCaT 细胞)中胸腺和激活调节趋化因子(TARC)和巨噬细胞来源的趋化因子(MDC)的产生。通过 DPPH 分析和 DCFH-DA 分析来证明 BCL 的免疫调节作用。我们发现 BCL 在 HaCaT 细胞中具有很强的清除 ROS 的作用。BCL 还显示出抑制 IFN-γ诱导的 TARC 和 MDC 的表达、NF-κB 的激活,并且显著阻断 IFN-γ诱导的 IκB 的降解和磷酸化。然而,它对 p38 MAPK 的磷酸化没有影响。总之,这些结果表明,BCL 通过抑制 Th2 趋化因子,可能对特应性皮炎等皮肤病具有治疗潜力,这至少部分归因于其抗氧化能力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0f2/3137989/eee6f74164dc/ECAM2012-617494.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0f2/3137989/e74d53a44cf9/ECAM2012-617494.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0f2/3137989/0dfd10617c4e/ECAM2012-617494.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0f2/3137989/ced3a4e9935a/ECAM2012-617494.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0f2/3137989/eee6f74164dc/ECAM2012-617494.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0f2/3137989/e74d53a44cf9/ECAM2012-617494.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0f2/3137989/0dfd10617c4e/ECAM2012-617494.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0f2/3137989/ced3a4e9935a/ECAM2012-617494.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0f2/3137989/eee6f74164dc/ECAM2012-617494.004.jpg

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