scholarly journals Expression and clinical significance of serum amyloid�A and interleukin‑6 in patients with acute exacerbation of chronic obstructive pulmonary disease

Author(s):  
Yongtao Wei ◽  
Songxia Wang ◽  
Dongping Wang ◽  
Cheng Liu
Author(s):  
Marta Maskey-Warzęchowska ◽  
Renata Rubinsztajn ◽  
Tadeusz Przybyłowski ◽  
Krzysztof Karwat ◽  
Patrycja Nejman-Gryz ◽  
...  

2008 ◽  
Vol 177 (3) ◽  
pp. 269-278 ◽  
Author(s):  
Steven Bozinovski ◽  
Anastasia Hutchinson ◽  
Michelle Thompson ◽  
Lochlan MacGregor ◽  
James Black ◽  
...  

Molecules ◽  
2019 ◽  
Vol 24 (10) ◽  
pp. 2020 ◽  
Author(s):  
Kiram Lee ◽  
Jin Choi ◽  
Bo Kyong Choi ◽  
Young-Mi Gu ◽  
Hyung Won Ryu ◽  
...  

Chronic obstructive pulmonary disease (COPD) is a major inflammatory lung disease characterized by irreversible and progressive airflow obstruction. Although corticosteroids are often used to reduce inflammation, steroid therapies are insufficient in patients with refractory COPD. Both serum amyloid A (SAA) and IL-33 have been implicated in the pathology of steroid-resistant lung inflammation. Picroside II isolated from Pseudolysimachion rotundum var. subintegrum (Plantaginaceae) is a major bioactive component of YPL-001, which has completed phase-2a clinical trials in chronic obstructive pulmonary disease patients. In this study, we investigated whether picroside II is effective in treating steroid refractory lung inflammation via the inhibition of the SAA-IL-33 axis. Picroside II inhibited LPS-induced SAA1 expression in human monocytes, which are resistant to steroids. SAA induced the secretion of IL-33 without involving cell necrosis. Picroside II, but not dexamethasone effectively inhibited SAA-induced IL-33 expression and secretion. The inhibitory effect by picroside II was mediated by suppressing the mitogen-activated protein kinase (MAPK) p38, ERK1/2, and nuclear factor-κB pathways. Our results suggest that picroside II negatively modulates the SAA-IL-33 axis that has been implicated in steroid-resistant lung inflammation. These findings provide valuable information for the development of picroside II as an alternative therapeutic agent against steroid refractory lung inflammation in COPD.


2016 ◽  
Vol 2016 ◽  
pp. 1-17 ◽  
Author(s):  
Xiaofan Lu ◽  
Ya Li ◽  
Jiansheng Li ◽  
Haifeng Wang ◽  
Zhaohuan Wu ◽  
...  

Background. Sequential treatments of Chinese medicines for acute exacerbation of chronic obstructive pulmonary disease (AECOPD) risk window (RW) have benefits for preventing reoccurrences of AEs; however, the effects on pulmonary function, pulmonary, and systemic inflammatory biomarkers remain unclear.Methods. Cigarette-smoke/bacterial infections induced rats were randomized into Control, COPD, AECOPD, Tongsai Granule/normal saline (TSG/NS), moxifloxacin + salbutamol/NS (MXF+STL/NS), TSG/Bufei Yishen Granule (BYG), MXF+STL/STL, and TSG+MXF+STL/BYG+STL groups and given corresponding medicine(s) in AE- and/or RW phase. Body temperature, pulmonary function, blood cytology, serum amyloid A (SAA) and C-reactive protein (CRP), pulmonary histomorphology and myeloperoxidase (MPO), polymorphonuclear (PMN) elastase, interleukins IL-1β, IL-6, and IL-10, and tumor necrosis factor- (TNF-)αexpressions were determined.Results. Body temperature, inflammatory cells and cytokines, SAA, CRP, and pulmonary impairment were higher in AECOPD rats than stable COPD, while pulmonary function declined and recovered to COPD level in 14–18 days. All biomarkers were improved in treated groups with shorter recovery times of 4–10 days, especially in TSG+MXF+STL/BYG+STL group.Conclusion. Sequential treatments with Tongsai and Bufei Yishen Granules, during AECOPD-RW periods, can reduce inflammatory response and improve pulmonary function and shorten the recovery courses of AEs, especially the integrated Chinese and Western medicines.


2021 ◽  
Vol 2021 ◽  
pp. 1-13
Author(s):  
Xiaojun Li ◽  
Ya Li ◽  
Jing Mao ◽  
Qingqing Bian ◽  
Yinshuang Xuan ◽  
...  

Chronic obstructive pulmonary disease (COPD) changes the structure of the intestinal microbiota and activates the acute exacerbation of COPD (AECOPD). Previous studies showed that the way to treat COPD and AECOPD via combination of Chinese and Western medicine was successful. However, the effect of the intervention on the structure of the intestinal microbiota has not been studied. In this study, we collected feces from model rats following intervention, integrated with Chinese and Western medicine, and used 16S rRNA gene sequencing to clarify the effect on intestinal microbiota. Methods. Twenty-five rats were randomized into the control, COPD, AECOPD, Western medicine (moxifloxacin hydrochloride tablets + salbutamol sulfate tablets, MXF/STL), and integrated Chinese and Western medicine (Tong Sai granules + moxifloxacin hydrochloride tablets + salbutamol sulfate tablets + Bu Fei Yi Shen granules + salbutamol sulfate tablets, TMS/FS) groups. Lipopolysaccharide-combined cigarette smoke exposure method was used to simulate the acute exacerbation-stabilization of COPD. Then, the model rats were intervened. Results. The intervention of combination Chinese and Western medicine improved the lung function, decreased the C-Reactive Protein (CRP) and Serum Amyloid A (SAA), and relieved pathological damage to the pulmonary alveoli and intestinal mucous of AECOPD rats. The proportion of Firmicutes, TM7, Oscillospira, Clostridium, Ruminococcus, Blautia, Treponema, and Turicibacter decreased, whereas that of Bacteroidetes, Proteobacteria, Lactobacillus, and Allobaculum increased via the intervention with the combination of Chinese and Western medicine. Conclusions. The intervention with Chinese and Western medicine optimizes the intestinal microbiota structure in AECOPD rat model, which provides a basis for the COPD study in the Chinese medicine.


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