Department of General Practice, the Second Affiliated Hospital of Zhejiang University Medical College, Hangzhou 310006, China.
Chin J Integr Med. 2013 Apr;19(4):282-8. doi: 10.1007/s11655-013-1410-1. Epub 2013 Jan 15.
To investigate the effect of Tripterygium polyglycosid on establishing airway eosinophil infiltration and related airway hyperresponsiveness of asthmatic mice.
A mature murine asthmatic model was made with ovabulmin sensitized and challenged C57BL/6 mice. Forty mice were divided into four groups with 10 mice in each group: mice sensitized and challenged with saline (WS group), mice sensitized and challenged with ovalbumin (WO group), mice sensitized and challenged with ovalbumin and treated with Tripterygium polyglycosid (TP group) and Dexamethasone (DXM group). The mice were intraperitoneally injected with 20 μg chicken ovabulmin emulsified in injected alum on days 0 and 14, then were challenged with an aerosol generated from 1% ovabulmin on days 24, 25 and 26. Tripterygium polyglycosid was injected intraperitoneally at 50 mg/kg on days 25, 26 and 27 after ovabulmin challenge. Dexamethasone was administrated to mice at 2 mg/kg on day 21, 23 before ovabulmin challenge. The airway hyperresponsiveness, mucus production, eosinophils in parabronchial area and bronchoalveolar lavage fluid and the level of interleukin-5, granulo-macrophage clone stimulating factor in bronchoalveolar lavage fluid were measured as indexes of inflammation.
Tripterygium polyglycosid treatment after ovabulmin challenge completely inhibited eosinophil infiltration in bronchoalveolar lavage fluid [(0.63 ± 0.34)× 10(4) vs. (75.0 ± 14.8)× 10(4), P<0.05] and the peribrochial area (12.60 ± 3.48 mm(2) vs. 379.0 ± 119.3 mm(2), P<0.05), mucus overproduction in airway (2.8 ± 1.7 vs. 7.1±5.6, P<0.05), and increased interleukin-5 levels in bronchoalveolar lavage fluid (28.8 ± 2.8 pg/mL vs. 7.5 ± 3.5 pg/mL, P<0.05). Meanwhile, Tripterygium polyglycosid treatment after ovabulmin challenge also partially inhibited airway hyperresponsiveness. The level of granulo-macrophage clone stimulating factor in bronchoalveolar lavage fluid didn't change with drugs intervention.
The administration of Tripterygium polyglycosid could inhibit the established airway inflammation and reduce the airway hyperresponsiveness of allergic asthmatic mice. It provides a possible alternative therapeutic for asthma.
研究雷公藤多苷对建立哮喘小鼠气道嗜酸性粒细胞浸润及相关气道高反应性的影响。
采用卵白蛋白致敏和激发 C57BL/6 小鼠建立成熟的哮喘小鼠模型。将 40 只小鼠分为 4 组，每组 10 只：生理盐水致敏和激发组（WS 组）、卵白蛋白致敏和激发组（WO 组）、卵白蛋白致敏和激发并用雷公藤多苷治疗组（TP 组）、地塞米松治疗组（DXM 组）。在第 0 天和第 14 天，用 20μg 鸡卵白蛋白乳化在注射用 alum 中，给小鼠腹腔注射，在第 24、25 和 26 天，用 1%卵白蛋白雾化激发。在卵白蛋白激发后第 25、26 和 27 天，用 50mg/kg 的雷公藤多苷腹腔注射。在卵白蛋白激发前第 21、23 天，用 2mg/kg 的地塞米松治疗小鼠。气道高反应性、气道黏液分泌、支气管旁区嗜酸性粒细胞和支气管肺泡灌洗液中的白细胞介素-5、粒细胞-巨噬细胞集落刺激因子水平作为炎症指标进行测量。
卵白蛋白激发后用雷公藤多苷治疗完全抑制了支气管肺泡灌洗液中的嗜酸性粒细胞浸润[（0.63±0.34）×104 对（75.0±14.8）×104，P<0.05]和支气管旁区（12.60±3.48mm2 对 379.0±119.3mm2，P<0.05）、气道黏液过度分泌（2.8±1.7 对 7.1±5.6，P<0.05），并增加了支气管肺泡灌洗液中的白细胞介素-5 水平（28.8±2.8pg/ml 对 7.5±3.5pg/ml，P<0.05）。同时，卵白蛋白激发后用雷公藤多苷治疗也部分抑制了气道高反应性。支气管肺泡灌洗液中粒细胞-巨噬细胞集落刺激因子的水平没有因药物干预而改变。
雷公藤多苷的给药可抑制已建立的气道炎症，降低过敏性哮喘小鼠的气道高反应性。为哮喘的治疗提供了一种可能的替代方法。
