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小青龙汤通过抑制自噬减轻大鼠慢性阻塞性肺疾病

Xiaoqinglong Decoction Attenuates Chronic Obstructive Pulmonary Disease in Rats via Inhibition of Autophagy.

作者信息

Wang Huanan, Mao Bing, Chen Chang

机构信息

Department of Integrated Traditional Chinese and Western Medicine, West China Hospital of Sichuan University, Chengdu 610041, China.

Institute of Life Sciences, Chongqing Medical University, Chongqing 400016, China.

出版信息

Evid Based Complement Alternat Med. 2018 Jan 31;2018:6705871. doi: 10.1155/2018/6705871. eCollection 2018.

DOI:10.1155/2018/6705871
PMID:29636783
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5831972/
Abstract

Effective treatment for chronic obstructive pulmonary disease (COPD) and knowledge of the underlying mechanism are urgently required. Xiaoqinglong decoction (XQL) is widely used to treat COPD in Traditional Chinese Medicine, but the mechanism remains unclear. In this study, we tested the hypothesis that XQL ameliorates COPD via inhibition of autophagy in lung tissue on a rat model. Rats were divided into five groups, namely, Control group, COPD group, COPD + XQL group, COPD + Rapamycin group, and COPD + XQL + Rapamycin group. Pathological changes on cellular and molecular levels, apoptosis reflected by TdT-mediated dUTP Nick-End Labeling (TUNEL) assay, and autophagy represented by LC3II/LC3I ratio and p62 level were investigated for each group. Compared with the Control group, COPD rats exhibited structural changes and activated inflammation in the lung tissue, together with enhanced apoptosis and elevated autophagy biomarkers. XQL treatment significantly ameliorated these changes, while rapamycin augmented them. These data altogether confirmed the involvement of autophagy in the pathogenesis of COPD and suggested that XQL attenuates COPD via inhibition of autophagy.

摘要

迫切需要有效的慢性阻塞性肺疾病(COPD)治疗方法以及对其潜在机制的了解。小青龙汤(XQL)在中医中广泛用于治疗COPD,但其机制尚不清楚。在本研究中,我们在大鼠模型上检验了XQL通过抑制肺组织自噬来改善COPD的假说。将大鼠分为五组,即对照组、COPD组、COPD + XQL组、COPD + 雷帕霉素组和COPD + XQL + 雷帕霉素组。对每组进行细胞和分子水平的病理变化、通过TdT介导的dUTP缺口末端标记(TUNEL)法反映的细胞凋亡以及以LC3II/LC3I比值和p62水平表示的自噬研究。与对照组相比,COPD大鼠肺组织出现结构变化和炎症激活,同时细胞凋亡增加且自噬生物标志物升高。XQL治疗显著改善了这些变化,而雷帕霉素则加剧了这些变化。这些数据共同证实了自噬参与COPD的发病机制,并表明XQL通过抑制自噬减轻COPD。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c679/5831972/ec3de91f1901/ECAM2018-6705871.004.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c679/5831972/adf8269cdb0f/ECAM2018-6705871.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c679/5831972/ec3de91f1901/ECAM2018-6705871.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c679/5831972/64ce931df71b/ECAM2018-6705871.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c679/5831972/2666b0249bcd/ECAM2018-6705871.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c679/5831972/adf8269cdb0f/ECAM2018-6705871.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c679/5831972/ec3de91f1901/ECAM2018-6705871.004.jpg

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