| Objective: To discuss the effects of Jade-Screen Powder(JSP) in asthmatic mouse model, through observing IL-13(Interleukin-13), IL-17, mi R-146 a, mi R-146 b, mi R-210, mi R-126 and mi R-21 a associated with modulated effects on helper T cells.Methods: Forty Balb/c mice were randomly divided into four groups of 10 mice each: normal control(group A), asthma model(group B), JSP treatment(group C) and dexamethasone treatment(group D). Mice were intraperitoneally injected with ovalbumin(OVA) to sensitizated on Day 0, Day 7 and Day 14 and challenged by OVA intranasally from Day 21 to Day 27 once a day to set allergic inflammation on both upper and lower airways. Normal control group and asthma model group were treated by normal saline once a day from Day 28 to Day 34, while JSP treatment group was treated by JSP and dexamethasone treatment group was treated by dexamethasone. IL-13 and IL-17 expression were detected from lung homogenates by ELISA. Hematoxylin and eosin staining was also performed to observe the pathological changes in lung tissue. The expressions of mi R-146 a, mi R-146 b, mi R-210, mi R-126 and mi R-21 a were detected by quantitative real time PCR(q Rt-PCR) from splenocytes.Results:(1)The higher level of IL-13 was found in asthma model group compared with that in normal control group(20.154±7.959ng/m L vs 8.746±2.492ng/m L, p<0.05). The expression of IL-13 in both JSP treatment group and dexamethasone treatment group was lower than asthma model group(6.382±1.691ng/m L vs 20.154±7.959ng/m L, p<0.01; 9.366±3.463ng/m L vs 20.154±7.959ng/m L, p<0.05, separately). And the level of IL-17 in asthma model group was significantly higher than normal control group(50.312±5.767ng/m L vs 31.696±2.836ng/m L, p<0.01). The level of IL-17 in both JSP treatment group and dexamethasone treatment group was significantly lower than asthma model group(24.212±1.247ng/m L vs 50.312±5.767ng/m L, p<0.01; 29.132±4.962ng/m L vs 50.312±5.767ng/m L, p<0.01, separately).(2)Lung tissue pathological changes: the lung tissue of normal control group was normal integrity, no stenosis of lumen and no inflammatory cells around. The pathological changes of asthma model group was found that the terminal respiratory tract was pseudostratified columnar epithelium and lots of inflammatory cell infiltrated in interstitial substance. The changes of JSP treatment group was mild alveolar collapse partially, improvement of respiratory tract epithelial cells hyperplasia and decreased of inflammatory cell infiltrating in submucosal. The lung tissue pathological changes of dexamethasone treatment group improved basically.(3)Upregulation of mi R-210 was observed in JSP group compared with that in asthma model group(2.052±0.871 vs 4.034±1.379, 3.95 fold, p<0.05). Meantime, the expression of mi R-126 in JSP and dexamethasone groups were increased relative to asthma model group(4.920±0.924 vs 6.024±0.447, 2.15 fold, p<0.05 and 3.862±1.510 vs 6.024±0.447, 4.48 fold, p<0.05, separately). And the expression of mi R-126 in asthma model group was 0.15 times of normal control group(6.024±0.447 vs 3.312±0.237, p<0.01). Similarly, the expression of mi R-126 in JSP group was lower than that in normal control group(4.920±0.924 vs 3.312±0.237, 0.33 fold, p<0.01).(4)Although the expression of mi R-146 a and mi R-146 b showed no significant difference in each group. The expression of mi R-146 a upregulated and the expression of mi R-146 b downregulated in asthma model group compared with that in normal control group.Both JSP group and dexamethasone treatment group improved the expression of mi R-146 a and mi R-146 b closing to the expression in normal control group.Conclusions:(1)Th2 and Th17 cells participated in the pathogenesis of asthma and the asthmatic process could be inhibited by dexamethasone and JSP.(2)JSP inhibited the Th17 cell to regulate the asthma by mi R-210 and mi R-126. |
PDF Full Text Request