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补中益气汤对NF-κB和Nrf2的差异调节与抑制肺部炎症相关。

Differential Regulation of NF-B and Nrf2 by Bojungikki-Tang Is Associated with Suppressing Lung Inflammation.

作者信息

Park Soo Ryun, Kim Kyun Ha, Kwun Min Jung, Lee Ji Yeon, Won Ran, Han Chang Woo, Choi Jun Yong, Joo Myungsoo

机构信息

School of Korean Medicine, Pusan National University, Yangsan 50612, Republic of Korea.

Department of Biomedical Laboratory Science, Division of Health Sciences, Dongseo University, Busan 47011, Republic of Korea.

出版信息

Evid Based Complement Alternat Med. 2018 Jan 30;2018:5059469. doi: 10.1155/2018/5059469. eCollection 2018.

DOI:10.1155/2018/5059469
PMID:29636779
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5831875/
Abstract

Bojungikki-tang (BT), an Asian herbal remedy, has been prescribed to increase the vitality of debilitated patients. Since a compromised, weakened vitality often leads to illness, BT has been widely used to treat various diseases. However, little is known about the mechanism by which BT exerts its effect. Given that BT ameliorates inflammatory pulmonary diseases including acute lung injury (ALI), we investigated whether BT regulates the function of key inflammatory factors such as NF-B and Nrf2, contributing to suppressing inflammation. Results show that BT interrupted the nuclear localization of NF-B and suppressed the expression of the NF-B-dependent genes in RAW 264.7 cells. In similar experiments, BT induced the nuclear localization of Nrf2 and the expression of the Nrf2-dependent genes. In a lipopolysaccharide-induced ALI mouse model, a single intratracheal administration of BT to mouse lungs ameliorated alveolar structure and suppressed the expression of proinflammatory cytokine genes and neutrophil infiltration to mouse lungs. Therefore, our findings suggest that suppression of NF-B and activation of Nrf2, by which BT suppresses inflammation, are ways for BT to exert its effect.

摘要

补中益气汤(BT)是一种亚洲草药方剂,一直被用于增强虚弱患者的活力。由于活力受损、减弱往往会导致疾病,BT已被广泛用于治疗各种疾病。然而,关于BT发挥作用的机制知之甚少。鉴于BT可改善包括急性肺损伤(ALI)在内的炎症性肺部疾病,我们研究了BT是否调节关键炎症因子如NF-κB和Nrf2的功能,从而有助于抑制炎症。结果表明,BT阻断了NF-κB的核定位,并抑制了RAW 264.7细胞中NF-κB依赖性基因的表达。在类似实验中,BT诱导了Nrf2的核定位和Nrf2依赖性基因的表达。在脂多糖诱导的ALI小鼠模型中,向小鼠肺部单次气管内给予BT可改善肺泡结构,并抑制促炎细胞因子基因的表达以及中性粒细胞向小鼠肺部的浸润。因此,我们的研究结果表明,BT通过抑制NF-κB和激活Nrf2来抑制炎症,这是BT发挥作用的途径。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f91/5831875/4a7415b5e4e2/ECAM2018-5059469.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f91/5831875/174a9bd913f1/ECAM2018-5059469.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f91/5831875/854e9e9a79d3/ECAM2018-5059469.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f91/5831875/c13049f8d3c8/ECAM2018-5059469.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f91/5831875/b2c23dfacbc4/ECAM2018-5059469.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f91/5831875/4a7415b5e4e2/ECAM2018-5059469.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f91/5831875/174a9bd913f1/ECAM2018-5059469.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f91/5831875/854e9e9a79d3/ECAM2018-5059469.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f91/5831875/c13049f8d3c8/ECAM2018-5059469.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f91/5831875/b2c23dfacbc4/ECAM2018-5059469.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f91/5831875/4a7415b5e4e2/ECAM2018-5059469.005.jpg

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