ObjectiveTo investigate the effects of resveratrol on airway remodeling in mice with chronic asthma. MethodsTwenty-four female BALB/c mice were randomly divided into three groups (8 mice in each group), namely a control group, an asthma group and a resveratrol (RV) group. All mice were sensitized with ovalbumin (OVA). The sensitized mice were then challenged with OVA while the control group were challenged with phosphate-buffered saline. The mice in the RV group were intraperitoneally injected with RV 30 min before OVA challenge, while the mice in the control and the asthma group were intraperitoneally injected with equal volume of dimethylsulfoxide. Periodic acid-Schiff (PAS) staining was performed to evaluate goblet cell hyperplasia, and Masson-trichrome staining was used to evaluate the deposition of collagen matrix. In addition, immunohistochemical analysis of the α-smooth muscle actin (α-SMA) was applied to examine airway smooth muscle cell hyperplasia and hypertrophy. The positive staining with PAS, Masson, α-SMA areas (μm 2/μm) of per bronchial basement membrane perimeter was used to indicate the degree of airway remodeling. ResultsIn the asthma group and the RV group, the degree of the goblet cell hyperplasia was significantly higher than that in the control group (5.44±1.13, 4.18±0.85vs. 0.00±0.00,P<0.01), and the level of goblet cell hyperplasia in the RV group was lower than that in the asthma group (P<0.05). The Masson staining showed that the deposition of collagen in the asthma group and the RV group was significantly higher than that in the control group (9.80±2.78, 5.71±0.68vs. 1.67±0.65,P<0.01), and the collagen deposition in the RV group was further lower than that in the asthma group (P<0.01). The α-SMA immunohistochemical analysis demonstrated that the expression of α-SMA in the asthma group and the RV group was significantly higher than that in the control group (10.39±1.65, 7.57±1.98vs. 2.41±1.06,P<0.01), and the level of α-SMA in the RV group was also lower than that in the asthma group (P<0.05). ConclusionThese findings suggest that resveratrol has an inhibitory effect on the process of airway remodeling in mice with chronic asthma.
ObjectiveTo investigate the role of acetyl CoA carboxylase (ACC)-induced Th17 development in the pathogenesis of asthma.MethodsA total of 24 C57BL/6 mice were randomly assigned to 4 groups (6 in each group), namely a normal group, an asthma group, a DMSO control group and an ACC inhibitor group. The mice in the asthma group, the DMSO control group and the ACC inhibitor group were sensitized and challenged with ovalbumin (OVA) to establish a model of acute asthma, the mice in the normal group were administrated with equal volume of phosphate buffered saline (PBS). The mice in the ACC inhibitor group were intraperitoneally administrated with TOFA, an ACC inhibitor (dissolved in DMSO firstly, then diluted with PBS solution) twice a week, while the DMSO control group were intraperitoneally administrated with equal concentration of DMSO. All mice were sacrificed 24 days later, then lung tissue and serum were collected. The inflammatory cells infiltrated in lung tissue were assessed by the means of HE staining under light microscope. The total level of IgE in serum was detected by ELISA. The percentage of Th17 cells in CD4+ T cells in lung tissue was evaluated by flow cytometry.ResultsThe inflammatory cells infiltration in the asthma group, the DMSO control group and the ACC inhibitor group increased significantly compared with that of the normal group (3.50±0.14, 3.47±0.08, 2.07±0.20vs. 0.50±0.17, allP<0.001), but there were no significant differences between the DMSO control group group and the asthma group (P>0.05), while administration of TOFA could significantly decrease the inflammatory cells infiltration (P<0.001). The total level of serum IgE in the asthma group, the DMSO control group and the ACC inhibitor group was significantly higher than that in the normal group [(5 680.40±831.40) ng/ml, (5 624.79±365.50) ng/ml, (2 028.95±134.60) g/mlvs. (400.52±57.13) ng/ml, allP<0.008], but there were no significant differences between the DMSO control group and the asthma group (P>0.05), while the total level of serum IgE in the ACC inhibitor group was significantly lower than that in the asthma group (P<0.008). The percentage of Th17 cells in CD4+ T cells in lung tissue increased markedly in the asthma group, the DMSO control group and the ACC inhibitor group compared with the normal group [(2.01±0.12)%, (1.95±0.16)%, (0.82±0.04)%vs. (0.59±0.03)%, bothP<0.008], and also there were no significant differences between the DMSO control group and the asthma group (P>0.05), while administration of TOFA could notably reduce the percentage of Th17 cells (P<0.008).ConclusionInhibition of ACC significantly alleviates the airway inflammation of OVA-induced asthma, and reduces the percentage of Th17 cells in lung tissue and the total level of serum IgE. ACC may participate in the pathogenesis of asthma by inducing Th17 development.