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作 者:王哲[1] 于柳[1] 龚锡平[1] 杨靖[1] 何敏[1] 武志强[1] 潘星[1] 曾南[1]
机构地区:[1]成都中医药大学药学院,中药资源系统研究与开发利用省部共建国家重点实验室培育基地,成都611137
出 处:《中国药学杂志》2014年第11期963-966,共4页Chinese Pharmaceutical Journal
基 金:国家自然科学基金资助项目(30973923);人社部高层次留学人才回国资助项目;留学回国人员科技活动择优资助项目(人社部人社厅函[2010]411、412号);2011年度四川省教育厅中药学专业综合改革大学生创新性实验项目
摘 要:目的从花生四烯酸代谢、一氧化氮/一氧化氮合酶(NO/NOS)通路及血清免疫球蛋白E水平角度,探讨荆防散乙酸乙酯提取部位的抗过敏作用机制。方法采用卵白蛋白合并百白破疫苗致小鼠主动全身过敏反应模型,荆防散乙酸乙酯提取物10.01、6.67 g·kg-1连续灌胃给药14 d,测定模型小鼠胸腺指数、脾脏指数,酶联免疫吸附法测定血清总免疫球蛋白E、白细胞三烯B4水平及肺组织一氧化氮、诱导型一氧化氮合酶、白细胞三烯B4水平,紫外分光光度法测定肺组织前列腺素E2水平。结果荆防散乙酸乙酯提取物6.67 g·kg-1显著降低模型小鼠的胸腺、脾脏指数(P<0.05),明显降低血清免疫球蛋白E、白细胞三烯B4水平及肺组织一氧化氮、白细胞三烯B4及前列腺素E2水平(P<0.05);提取物10.01、6.67 g·kg-1均能显著降低肺组织诱导型一氧化氮合酶水平(P<0.05)。结论荆防散乙酸乙酯提取物具有抗过敏作用,作用机制与减少免疫球蛋白E的生成,抑制炎性过敏介质一氧化氮、白细胞三烯B4及前列腺素E2的释放有关。OBJECTIVE To investigat the mechanism of anti-anaphylaxis effect of Jing-fang powder ( traditional Chinese medicines) by using initiative systemic anaphylaxis model in mice. METHODS The modal of initiative systemic anaphylaxis in mice was induced by intraperitoneal injection with ovalbumin and DPT vaccine, and the ethyl acetate extraction of Jing-fang powder was intragastricly administrated for 14 d. ELISAs methods were used to measure the levels of total IgE and LTB4 in serum, and the levels of NO, iNOS and LTB4 in lung tissues in model mice. Uhraviolet spectrophotometry was used to measure the PGE2level in lung tissue, and the index of thymus and spleen were also evaluated. RESULTS At the dose of 6. 67 g · kg^-1, the ethyl acetate extraction of Jing-fang powder decreased the index of thymus and spleen ( P 〈 0.05 ) , as well as suppressed the production of total IgE and LTB4 in serum (P 〈0. 05, and reduced the levels of NO, iNOS, LTB4 and PGE2 in lung tissue in model miee(P 〈0.05). Meanwhile, the extraction also suppressed the activity of iNOS in lung tissue under the dose of 6. 67 and 10. 01 g · kg ^- 1 ( p 〈 0. 05 ). CONCLUSION These results suggest that the ethyl acetate extraction of Jing-fang Powder has potential anti-allergic effect, which the mechanism may be related to reduce the production of IgE, and inhibit the release of metabolic products of arachidonic acid, for example LTB4 and PGE2, and decrease the release of inflammatory allergy mediators NO.
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