雷公藤甲素通过IL-10/Th17细胞调节哮喘小鼠气道炎症

王爱利.雷公藤甲素通过IL-10/Th17细胞调节哮喘小鼠气道炎症[J].内科急危重症杂志,2019,25(4):331-334

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DOI：10.11768/nkjwzzzz20190421

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基金项目:武汉市卫计委项目（No:WZ16D05）

作者	单位	E-mail
王爱利	华中科技大学同济医学院附属武汉市中西医结合医院	Whyyy191@sina.com

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中文摘要:

目的：探索雷公藤甲素对哮喘小鼠外周血白细胞介素-10(IL-10)、辅助性T17(Th17)细胞及气道炎症的影响。方法：32只雌性BALB/c小鼠随机分为对照组、哮喘组、雷公藤甲素组、地塞米松组，每组8只。对照组给予生理盐水致敏与激发，哮喘组给予卵清蛋白(OVA)致敏及激发，雷公藤甲素组在每次激发前给予40μg/（kg•d）雷公藤甲素腹腔注射干预，地塞米松组在每次激发前给予1mg/（kg•d）地塞米松腹腔注射干预。最后一次激发24h后收集各组小鼠肺泡灌洗液进行细胞分类计数，检测外周血细胞因子IL 10、外周血CD4+淋巴细胞中Th17细胞比例，对肺组织进行HE染色,评估小鼠气道炎症的变化。结果: 哮喘组小鼠IL 10浓度明显低于对照组，Th17细胞比例明显高于对照组，且肺泡灌洗液细胞总数、嗜酸性粒细胞计数、中性粒细胞计数、气道周围炎症评分均明显高于对照组（均P<0.01）。雷公藤甲素组及地塞米松组IL 10浓度较哮喘组明显升高，Th17细胞比例较哮喘组明显下降，且肺泡灌洗液细胞总数、嗜酸性粒细胞计数、中性粒细胞计数、气道周围炎症评分明显低于哮喘组（均P<0.05），而雷公藤甲素组及地塞米松组之间上述指标比较差异无统计学意义（均P>0.05）。结论：雷公藤甲素可能通过IL 10对Th17细胞的调节作用减轻气道周围炎症，为哮喘的临床治疗提供新的靶点。

英文摘要:

Objective: To investigate the effects of triptolide on IL-10, Th17 cells in peripheral blood and airway inflammation in asthmatic mice. Methods: Thirty-two female BABL/c mice were randomly divided into four groups with 8 in each group. Mice in control group were treated with saline, those in asthmatic group were sensitized and challenged with OVA, those in triptolide group were sensitized and challenged with OVA and given triptolide (40 μg/kg every day) intraperitoneally prior to the challenge, and those in dexamethasone group received dexamethasone (1mg/kg every day) intraperitoneally before challenge. The BALF of each group was collected 24h after the final OVA challenge for cells sorting and counting. The levels of IL-10 in peripheral blood and percentage of Th17 cells from peripheral blood CD4+T lymphocytes were detected by ELISA and flow cytometry respectively. The HE staining of lung tissue was performed to evaluate the airway inflammation. Results: The IL-10 level was significantly lower, and the percentage of Th17 cells was significantly higher in asthmatic group than those in control group (P<0.01). The HE staining of lung tissue indicated that the total cell number, and number of eosnophils and neutrophils in the BALF of asthmatic group were significantly greater than those in control group (P<0.01). Treatment with triptolide or dexamethasone greatly reduced the percentage of Th17 cells, increased IL-10 concentration and decreased cell sorting counts in BALF and airway inflammation scores. For indexes mentioned above, no significant differences between triptolide group and dexamethasone group were observed (P>0.05). Conclusions: Triptolide may alleviate airway inflammation in asthmatic mice through the regulation of IL-10 on Th17 cells, providing a new target for the clinical treatment of asthma.