Oxidative/antioxidative imbalance and chronic inflammation are the main contributors to the pathogenesis of chronic obstructive pulmonary disease (COPD). This study evaluated the effect of recuperating lung decoction (RLD) on inflammation and oxidative stress in rats with COPD induced by cigarette smoke and lipopolysaccharides (LPS). We used intravenous infusion of LPS combined with cigarette smoke exposure as a COPD rat model. We observed that RLD treatment increased the protein level of GSH and the ratio of GSH/GSSG but decreased 8‐OHdG and 4‐HNE in the serum. Furthermore, RLD significantly inhibited the expressions of IL‐1β, IL‐6, TNF‐α, and TGF‐β induced by cigarette smoke exposure, reduced the number of inflammatory cells in the bronchoalveolar lavage fluid, and alleviated the severity of cigarette smoke‐induced emphysema. Mechanistically, RLD treatment prevented disease through downregulation of phosphorylated‐ERK and Nrf2 expression, which regulates the production of proinflammatory cytokines. RLD treatment exerted a dramatic therapeutic effect on COPD. This study revealed a mechanism that RLD functions on the regulation of ERK signalling to inhibit inflammation.

Coronary heart disease (CHD) is one of the most important types of heart disease because of its high incidence and mortality. With the era of systems biology bursting into reality, the analysis of the whole biological systems whether they are cells, tissues, organs, or the whole organisms has now become the norm of biological researches. Metabolomics is the branch of science concerned with the quantitative understandings of the metabolite complement of integrated living systems and their dynamic responses to the changes of both endogenous and exogenous factors. The aim of this study is to discuss the characteristics of plasma metabolites in CHD patients and CHD Qi deficiency syndrome patients and explore the composition and concentration changes of the plasma metabolomic biomarkers. The results show that 25 characteristic metabolites related to the CHD patients comparing with the healthy people, and 4 identifiable variables had significant differences between Qi deficiency and non‐Qi deficiency patients. On the basis of identifying the different plasma endogenous metabolites between CHD patients and healthy people, we further prompted the metabolic rules, pathogenesis, and biological essence in Qi deficiency syndrome patients.

Eosinophils (EOS) is one of the most important cells involved in the pathogenesis of chronic airway inflammation in asthma, and its apoptosis is part of the mechanisms of asthma. Therefore, this study aimed to observe the effect of Chinese medicine Wentong decoction (WTD) in EOS apoptosis in asthmatic rats. This work also explored the mechanism of WTD regulation in EOS apoptosis and provided a new target for clinical treatment of asthma. Asthmatic rats induced by ovalbumin were treated with WTD. Lung function of rats in each group was detected, and lung tissue pathology, EOS counts in blood and bronchoalveolar lavage fluid were observed. The degree of the EOS apoptosis in rats was detected. The expression content of interleukin (IL)-5, IL-10, chemokine (C–C motif) ligand 5 (CCL5), granulocyte–macrophage colony-stimulating factor (GM-CSF), transforming growth factor beta 1 (TGF-β1), interferon (IFN)-γ, and other cytokines in rat serum and the genes of Eotaxin mRNA, Fas mRNA, FasL mRNA, Fas/FasL and Bcl-2 mRNA in the lung tissues were determined. WTD can reduced airway resistance in rat models and improved airway compliance. The pathological changes of lung tissue in WTD group were significantly alleviated, at the same time, WTD could reduce the EOS count in the blood and BALF smears of the asthmatic model rats. Compared with the model group, the apoptosis degree of EOS significantly increased in rats in the WTD group. The expression of IL-5, CCL5, and GM-CSF in the serum and the expression of Eotaxin mRNA, Bcl-2 mRNA in the lung tissues in rats in the WTD group rats decreased. Moreover, the expression of IL-10, TGF-β1, and IFN-γ in the serum and the expression of Fas mRNA, FasL mRNA in the lung tissues in rats in the WTD group rats increased compared with that in rats in the model group. Wentong decoction may accelerate EOS apoptosis, reduce asthma inflammation, and alleviate the disease through regulating and controlling the factors related to the anti-apoptosis and pro-apoptosis.

Purpose/Objective. To evaluate the effects of Recuperating Lung Decoction (RLD) on the indices of oxidative stress in a rat model of COPD and detect the indices of the MAPK/AP‐1/γ‐GCS signal pathway for a further survey of the possible targeting site of RLD. Methods/Materials. The rats of COPD were treated with RLD. The protein levels of glutathione (GSH), oxidized glutathione (GSSG), 8‐hydroxy‐2‐deoxyguanosine (8‐OHdG), and 4‐hydroxynonenal (4‐HNE) were measured. In addition, the levels of key signaling molecules (extracellular signal‐regulated kinases [ERK], the c‐jun N‐terminal kinase [JNKs signal pathway], and p38 MAP kinase [p38MAPK], AP‐1 proteins [C‐fos, C‐jun], and γ‐glutamyl‐cysteine synthetase [γ‐GCS‐h]) of the MAPK/AP‐1/γ‐GCS‐h signal pathway were assessed. Results. After treatment, the protein level of GSH and the ratio of GSH/GSSG were increased and the amounts of 8‐OHdG and 4‐HNE were decreased significantly in lung tissues when compared with the nontreated COPD group. Further results showed that the RLD could effectively inhibit the MAPK pathway by inactivation of p38MAPK and ERK and could also downregulate the AP‐1 and the γ‐GCS‐h genes expressions in both protein and mRNA levels. Conclusion. RLD might improve the state of oxidative stress by downregulation of the expression of γ‐GCS‐h gene by inhibition of the MAPK/AP‐1 pathway, thereafter enhancing the ability of antioxidation in COPD.

Background: Chronic obstructive pulmonary disease (COPD) is a common chronic respiratory disease with increasing morbidity and mortality that cause huge social and economic loss. Although recommended by guidelines, pulmonary rehabilitation has not been widely applied in clinics because of its inherent limitations. Acupuncture therapy (AT) as one of the most popular treatments in traditional Chinese medicine has been used to treat COPD. We aim to evaluate the safety and efficacy of acupuncture in the treatment of COPD. Methods: Web of science, PubMed, Springer, Medline, Cochrane Library, EBASE, WHO International Clinical Trials Registry Platform (ICTRP), China National Knowledge Infrastructure Database (CNKI), Wan Fang Database, Chinese Scientific Journal Database (VIP), and Chinese Biomedical Literature Database will be searched from their inception to May 10, 2019. Randomized controlled trials that evaluated the safety and efficacy of acupuncture for the treatment on patients with COPD will be included. The primary outcome measures will include Dyspnea scores, lung function and blood eosinophils. The secondary outcome measures will include St George's Respiratory Questionnaire and 6-minute walk distance. Study selection, data extraction, and risk of bias assessment will be independently undertaken, respectively. Statistical analysis will be conducted by RevMan software (version 5.3). Results: This study will provide high-quality synthesis based on current evidence of acupuncture treatment for COPD in several aspects, including symptom score, quality of life score, side effects and laboratory examination, such as lung function text, blood eosinophils (EOS) etc. Conclusion: The results of this study will provide updated evidence for weather acupuncture is an effective and safe intervention for COPD. Ethics and dissemination: It is not necessary for this systematic review to acquire an ethical approval. This review will be disseminated in a peer-reviewed journal or conference presentation. PROSPERO registration number: PROSPERO CRD42019136087.