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补肺益肾颗粒联合电针通过调节TLR-4/NF-κB信号通路对慢性阻塞性肺疾病大鼠的影响

Effect of Bufei Yishen Granules Combined with Electroacupuncture in Rats with Chronic Obstructive Pulmonary Disease via the Regulation of TLR-4/NF-B Signaling.

作者信息

Ma Jindi, Tian Yange, Li Jiansheng, Zhang Lanxi, Wu Mingming, Zhu Lihua, Liu Shuai

机构信息

Dongzhimen Hospital, Beijing University of Chinese Medicine, Beijing 100700, China.

Collaborative Innovation Center for Respiratory Disease Diagnosis and Treatment & Chinese Medicine Development of Henan Province, Henan University of Chinese Medicine, Zhengzhou, Henan 450046, China.

出版信息

Evid Based Complement Alternat Med. 2019 May 29;2019:6708645. doi: 10.1155/2019/6708645. eCollection 2019.

DOI:10.1155/2019/6708645
PMID:31275415
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6560336/
Abstract

BACKGROUND

The combined therapy of Bufei Yishen granules (BY) and electroacupuncture (EA) has shown good effects clinically in treating chronic obstructive pulmonary disease (COPD). The present study aimed to observe the effects of the BY + EA combination in a COPD rat model and dissect the potential mechanisms via Toll-like receptor (TLR) 4/nuclear factor kappa B (NF-B) signaling.

METHODS

The COPD rats were treated with normal saline, aminophylline, Bufei Yishen granules, electroacupuncture, or Bufei Yishen granules combined with electroacupuncture. The pulmonary function; lung tissue histology; levels of inflammatory factors; expression levels of TLR-4, inhibitor of nuclear factor kappa B (IB), and NF-B; and activation of NF-B in the lung tissues were evaluated.

RESULTS

Pulmonary function was markedly decreased in the COPD rats, and the lung tissue histology of the COPD rats showed severe pathological changes. The pulmonary function and lung tissue morphology in the treatment groups (APL, BY, EA, and BY + EA) were improved. The increased levels of the inflammatory cytokines interleukin (IL)-1 and IL-6 indicated a chronic inflammatory state in the COPD rats. In the BY, EA, and BY + EA groups, the levels of IL-1 and IL-6 were decreased, especially in the BY + EA group. In addition, the mRNA and protein expression levels of TLR-4, IB, and NF-B were obviously downregulated in the BY and BY + EA groups; and the NF-B p65 activation was significantly decreased in the BY, EA, and BY + EA groups.

CONCLUSIONS

Bufei Yishen granules and electroacupuncture have curative effects in COPD rats, and the combination therapy of Bufei Yishen granules and electroacupuncture is superior. The TLR-4/NF-B pathway may be involved in the potential mechanisms by which Bufei Yishen granules and electroacupuncture reduce inflammation.

摘要

背景

补肺益肾颗粒(BY)联合电针(EA)在临床治疗慢性阻塞性肺疾病(COPD)中显示出良好疗效。本研究旨在观察BY+EA联合治疗对COPD大鼠模型的影响,并通过Toll样受体(TLR)4/核因子κB(NF-κB)信号通路剖析其潜在机制。

方法

将COPD大鼠分别用生理盐水、氨茶碱、补肺益肾颗粒、电针或补肺益肾颗粒联合电针进行治疗。评估肺功能、肺组织组织学、炎症因子水平、TLR-4、核因子κB抑制蛋白(IκB)和NF-κB的表达水平,以及肺组织中NF-κB的激活情况。

结果

COPD大鼠肺功能明显降低,肺组织组织学显示严重病理改变。治疗组(氨茶碱、BY、EA和BY+EA)的肺功能和肺组织形态得到改善。炎症细胞因子白细胞介素(IL)-1和IL-6水平升高表明COPD大鼠处于慢性炎症状态。在BY、EA和BY+EA组中,IL-1和IL-6水平降低,尤其是在BY+EA组。此外,BY和BY+EA组中TLR-4、IκB和NF-κB的mRNA和蛋白表达水平明显下调;BY、EA和BY+EA组中NF-κB p65激活明显降低。

结论

补肺益肾颗粒和电针对COPD大鼠有治疗作用,且补肺益肾颗粒与电针联合治疗效果更佳。TLR-4/NF-κB通路可能参与补肺益肾颗粒和电针减轻炎症的潜在机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7cf6/6560336/81ebe79a14d5/ECAM2019-6708645.008.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7cf6/6560336/81ebe79a14d5/ECAM2019-6708645.008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7cf6/6560336/b4203807d181/ECAM2019-6708645.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7cf6/6560336/317fadfa5f42/ECAM2019-6708645.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7cf6/6560336/ccba290b970d/ECAM2019-6708645.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7cf6/6560336/3e5f369e3cac/ECAM2019-6708645.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7cf6/6560336/c149c8f44e72/ECAM2019-6708645.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7cf6/6560336/210d8fd8bc40/ECAM2019-6708645.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7cf6/6560336/f26e3d48e385/ECAM2019-6708645.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7cf6/6560336/81ebe79a14d5/ECAM2019-6708645.008.jpg

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