ObjectiveTo investigate the effects of smoking on Th17/Treg T cell subsets and cytokines expression in patients with chronic obstructive pulmonary disease (COPD) in stable stage. MethodsFrom February 2012 to June 2013, sixty outpatients with stable COPD (20 cases of non-smokers, 40 cases of smokers) and 15 normal volunteers were recruited in the study in the Traditional Chinese Medicine Hospital affiliated to Xinjiang Medical University. Th17/Treg level in peripheral blood was detected by flow cytometry method. Cytometric bead array system was used to detect TGF-β, IL-10, IL-17A, IFN-γand other inflammatory factors in serum. ResultsThe patients' age, duration of disease, lung function, disease severity, and other related data were comparable between the smoking COPD group and the non-smoking COPD group (P > 0.05). Th17/Treg level was increased in the smoking COPD group compared with the normal group (P < 0.05), and showed an increasing trend from the normal group to the non-smoking COPD group and the smoking COPD group. The level of IL-2 in the smoking and non-smoking COPD groups was lower than that in the normal group. Compared with the normal group, the level of TNF-αwas significantly decreased in the smoking and non-smoking COPD groups(P < 0.05). ConclusionsSystemic inflammatory response continuously exists in patients with COPD even in the stable phase. Smoking can partly enhance the inflammatory reaction in COPD. The Th17/Treg T cell subsets associated cytokine regulation has gradually tended to a balance in the stable phase, and inflammatory factors related recovery speed is not consistent, suggesting that smoking may play a certain role in the recovery of balance.
ObjectiveTo study the protective effect and mechanism of ophiopogonin D (OP-D) on lipopolysaccharide induced acute lung injury (ALI) in mice.MethodsFifty SPF C57BL/6 mice were randomly divided into five groups, ie. a control group, a sham operation group, a model group, an OP-D group (10 mg·kg–1·d–1), and a dexamethasone group (2 mg·kg–1·d–1), with 10 mice in each group. One day before the establishment of the model, the OP-D group and the dexamethasone group received the corresponding drugs by gavage. The model group, the OP-D group and the dexamethasone group received lipopolysaccharide (2 mg/kg, 30 μL) through the trachea to establish the ALI model. The sham operation group received the same volume of normal saline. The blank control group was not treated. Six hours after the operation, the mice were weighed and then killed for peripheral blood and lung tissue. The weight of lung tissue was measured to evaluate the degree of pulmonary edema; the pathological changes of lung tissue were observed by hematoxylin-eosin staining; the mRNA expressions of interleukin (IL)-6, IL-10, and IL-17 in lung tissue were detected by qPCR; the percentage of Th17 and Treg cells in peripheral blood was detected by flow cytometry.ResultsCompared with the model group, the degree of pulmonary edema in the OP-D group decreased significantly (P<0.05), the lung tissue injury decreased, the mRNA expressions of IL-6 and IL-17 in the lung tissue and the proportion of Th17 cells in the peripheral blood decreased significantly (P<0.05), the proportion of Treg cells in the peripheral blood and the mRNA expression of IL-10 in the lung tissue increased significantly (P<0.05).ConclusionOP-D may have therapeutic effect on LPS induced ALI in mice by regulating the balance of Th17/Treg cells.