Abstract：
BACKGROUND: Ding-Chuan-Tang (Abbreviated as DCT) is frequently prescribed for treatment of respiratory diseases, including chronic obstructive pulmonary disease (COPD), which is characterized by coughing, wheezing, and chest tightness in traditional Chinese medicine (TCM). However, the potential mechanism of DCT has not been investigated.
OBJECTIVE: The aim of the study is to explore the efficiency of DCT in the treatment of COPD in vivo and in vitro, and to illustrate the possible mechanism against COPD.
METHODS: COPD model was induced by exposure of mice to cigarette smoke (CS) for 16 weeks. Enzyme-linked immunosorbent assay (ELISA), immunofluorescence assay, Western blot, etc., were used to explore the efficiency and mechanisms of DCT. Network pharmacology analysis, including Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis, etc., was performed to explore the potential targets in the treatment of DCT on COPD.
RESULTS: DCT significantly alleviated pulmonary pathological changes in mouse COPD model, and inhibited inflammatory response induced by CS and LPS in vivo and in vitro. Network pharmacology analysis suggested that DCT alleviated COPD via inhibiting inflammation by regulating PI3K-AKT pathway. In cell-based models, DCT suppressed the phosphorylation of PI3K and AKT, which further regulated its downstream targets Nrf2 and NF-κB, and inhibited inflammatory response.
CONCLUSIONS: DCT effectively attenuated COPD in the mouse model induced by CS. The therapeutic mechanism of DCT against COPD was closely associated with the regulation of PI3K-AKT pathway and its downstream transcription factors, Nrf2 and NF-κB.
OBJECTIVE: The aim of the study is to explore the efficiency of DCT in the treatment of COPD in vivo and in vitro, and to illustrate the possible mechanism against COPD.
METHODS: COPD model was induced by exposure of mice to cigarette smoke (CS) for 16 weeks. Enzyme-linked immunosorbent assay (ELISA), immunofluorescence assay, Western blot, etc., were used to explore the efficiency and mechanisms of DCT. Network pharmacology analysis, including Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis, etc., was performed to explore the potential targets in the treatment of DCT on COPD.
RESULTS: DCT significantly alleviated pulmonary pathological changes in mouse COPD model, and inhibited inflammatory response induced by CS and LPS in vivo and in vitro. Network pharmacology analysis suggested that DCT alleviated COPD via inhibiting inflammation by regulating PI3K-AKT pathway. In cell-based models, DCT suppressed the phosphorylation of PI3K and AKT, which further regulated its downstream targets Nrf2 and NF-κB, and inhibited inflammatory response.
CONCLUSIONS: DCT effectively attenuated COPD in the mouse model induced by CS. The therapeutic mechanism of DCT against COPD was closely associated with the regulation of PI3K-AKT pathway and its downstream transcription factors, Nrf2 and NF-κB.
摘要：
背景：丁川汤（缩写为DCT）经常用于治疗呼吸系统疾病，包括慢性阻塞性肺疾病（COPD），其特点是咳嗽，喘息,和胸闷在中医（TCM）。然而,DCT的潜在机制尚未得到研究。
目的：本研究的目的是探讨DCT在体内和体外治疗COPD的有效性，并说明抗COPD的可能机制。
方法：小鼠暴露于香烟烟雾（CS）16周诱导COPD模型。酶联免疫吸附测定(ELISA),免疫荧光测定，蛋白质印迹,等。,用于探索DCT的效率和机制。网络药理学分析，包括基因本体论(GO)，京都基因和基因组百科全书（KEGG）富集分析，等。,目的是探讨DCT治疗COPD的潜在靶点。
结果：DCT可显着减轻COPD模型小鼠肺部病理变化，并在体内外抑制CS和LPS诱导的炎症反应。网络药理学分析提示DCT通过调节PI3K-AKT通路抑制炎症反应减轻COPD。在基于单元的模型中，DCT抑制PI3K和AKT的磷酸化，进一步调控其下游靶点Nrf2和NF-κB，并抑制炎症反应。
结论：DCT可有效减轻CS诱导的小鼠模型中的COPD。DCT对COPD的治疗机制与PI3K-AKT通路及其下游转录因子的调控密切相关,Nrf2和NF-κB。
目的：本研究的目的是探讨DCT在体内和体外治疗COPD的有效性，并说明抗COPD的可能机制。
方法：小鼠暴露于香烟烟雾（CS）16周诱导COPD模型。酶联免疫吸附测定(ELISA),免疫荧光测定，蛋白质印迹,等。,用于探索DCT的效率和机制。网络药理学分析，包括基因本体论(GO)，京都基因和基因组百科全书（KEGG）富集分析，等。,目的是探讨DCT治疗COPD的潜在靶点。
结果：DCT可显着减轻COPD模型小鼠肺部病理变化，并在体内外抑制CS和LPS诱导的炎症反应。网络药理学分析提示DCT通过调节PI3K-AKT通路抑制炎症反应减轻COPD。在基于单元的模型中，DCT抑制PI3K和AKT的磷酸化，进一步调控其下游靶点Nrf2和NF-κB，并抑制炎症反应。
结论：DCT可有效减轻CS诱导的小鼠模型中的COPD。DCT对COPD的治疗机制与PI3K-AKT通路及其下游转录因子的调控密切相关,Nrf2和NF-κB。
