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作 者:刘维[1] 吴沅皞[2] 刘晓亚[1] 张磊[1] 薛斌[2]
机构地区:[1]天津中医药大学第一附属医院风湿免疫科,天津300193 [2]天津中医药大学研究生院,天津300193
出 处:《中国医学工程》2011年第4期1-3,6,共4页China Medical Engineering
基 金:国家自然科学基金项目(30772809)
摘 要:目的探讨解毒通络法对类风湿关节炎病理进展中炎性因子的控制作用。方法复制胶原诱导型关节炎(Collagen-induced Arthritis,CIA)大鼠模型,随机分为空白对照组,模型对照组,清痹片低剂量组、中剂量组、高剂量组,并以甲氨蝶呤治疗组作为阳性对照组,致炎第21天起每天给药干预。分别于35d和49d各处死一半动物,取踝关节行免疫组化法实验检测转化生长因子β1(TGFβ1)、肿瘤坏死因子α(TNFα)、白细胞介素1β(IL-1β)、基质金属蛋白酶3(MMP-3),比较各组间各炎性因子蛋白表达的差异。结果成功复制CIA模型,模型组TGFβ1、TNFα、IL-1β蛋白表达水平较空白组升高(P<0.01);清痹片各剂量组TGFβ1、TNFα、IL-1β及MMP-3表达水平均低于模型组,且显示出一定的量效关系;清痹片高剂量组TNFα、IL-1β、MMP-3表达水平低于MTX组(P<0.01),清痹片中剂量组与MTX比较差异无统计学意义(P>0.05)。结论证明活血通络法能明显下调胶原诱导型关节炎病变关节TGFβ1、TNFα、IL-1β及MMP-3水平,减轻炎症症状,控制类风湿关节炎的病理进展。【Objective】 The project intends to illuminate the possible effect of the dispelling toxins and dredging collaterals on the inflammatory factors in the rheumatoid arthritis process,as a scientific basis for the research and application of the anti-inflammatory traditional Chinese medicine.【Methods】 Focusing on the Qingbi Tablets with the formulating principle of dispelling toxins and dredging collaterals,under the guidance of TCM theory,the experimental research used collagen-induced arthritis(CIA) as the experimental animal models.Comparating with normal group,the CIA rats were divided randomly into 5 groups,treating with or without the Qingbi Tablets of low,middle,high dosage(0.36g/kg·d,1g/kg·d or 1.8g/kg·d) or the methotrexate from the 21th day.One half of rats were sacrificed on the 35th day or the 49th.The ankle joints were collected for measuring the TGFβ1,TNFα,IL-1β and MMP-3 with the immunohistochemistry assay.【Results】 The expression levels of TGFβ1、TNFα、IL-1β and MMP-3 of CIA in rats are higher significantly compared with the normal ones(P0.01).With a dose dependent,the expression levels of TGFβ1、TNFα、IL-1β、MMP-3 in treated groups are significantly lower than the model group(P0.01).【Conclusion】 The formulating principle of dispelling toxins and dredging collaterals has the effects of down-regulation on the expression of the TGFβ1,TNFαIL-1β and MMP-3 on the RA process effectively.
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