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作 者:田静[1,2] 李忻红[2] 朱卉雯[1,2] 马贤德[1] 冯常青[2] 王敏[2]
机构地区:[1]辽宁中医药大学,辽宁沈阳110032 [2]辽宁中医药大学附属医院,辽宁沈阳110032
出 处:《中国中医药信息杂志》2015年第7期47-50,共4页Chinese Journal of Information on Traditional Chinese Medicine
基 金:辽宁省教育厅高等学校科学研究项目(L2012342);辽宁省中医药学(专)科能力建设项目(2011-lnzyxzk-03)
摘 要:目的观察健脾养血祛风方对脾虚慢性湿疹模型小鼠皮损处水通道蛋白3(AQP3)含量的影响,并探讨其可能的作用机制。方法取健康雄性小鼠50只,随机分为正常组、模型组、阳性药组及中药高、低剂量组。采用小剂量反复DNCB涂抹及番泻叶致脾虚证建立小鼠脾虚慢性湿疹模型。中药组予健脾养血祛风方灌胃,阳性药组予盐酸左西替利嗪灌胃。免疫组化法检测病变皮肤组织中AQP3的表达,同时观察皮肤组织病理变化。结果病理观察结果显示,健脾养血祛风方对小鼠皮损处炎症损伤具有一定的修复作用。与正常组比较,模型组AQP3过度表达;与模型组比较,各给药组AQP3表达均明显下降,染色强度降低。模型组AQP3平均光密度值明显高于正常组(P<0.01);与模型组比较,各给药组均能下调AQP3表达(P<0.05)。结论健脾养血祛风方下调皮损中过度表达的AQP3可能是其治疗脾虚慢性湿疹的作用机制之一。Objective To observe the effects of Jianpi Yangxue Qufeng Formula (JPYXQF) on the AQP3 in mice with chronic eczema, and explore mechanism of action. Methods Fifty healthy male mice were randomly divided into 5 groups, namely normal group, model group, positive medicine group and JPYXQF high and low dose groups. Low-dose DNCB and Sennae Fominm were used to establish mice models of chronic eczema with spleen deficiency. JPYXQF groups were treated by JPYXQF for gavage, while the positive medicine group was treated by levocetirizine hydrochloride for gavage. The expression of AQP3 in mice skin tissue was detected by immunohistochemical method. At the same time, the pathological changes of skin were observed. Results The pathology of mice skin lesion showed that JPYXQF has certain recovery effects on the inflammation injury of skin lesion. Compared with the normal group, expression of AQP3 over expressed in model group. Compared with the model group, the expression of AQP3 in all treatment groups significantly decreased, and the staining intensity decreased. In the model group, the average optical density of AQP3 was significantly higher than that in the normal group (P〈0.01). Compared with the model group, the treatment groups can reduce the expression of AQP3 in mice skin tissues (P〈0.05). Conclusion JPYXQF can reduce the over expression of AQP3 in skin lesion, which is probably its mechanism for the treatment of chronic eczema.
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