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作 者:赵会勤 李超杰[1] 徐玉洁[1] 贾奥 贾贝西[1] 贾成军[2] ZHAO Huiqin LI Chaojie XU Yujie JIA Ao JIA Beixi JIA Chengjun(College of Pharmacy, Zhengzhou University, Zhengzhou 450001, China Henan Province Hospital of TCM, Zhengzhou 450002, China)
机构地区:[1]郑州大学药学院,河南郑州450001 [2]河南省中医院,河南郑州450002
出 处:《中国民族民间医药》2017年第5期37-41,共5页Chinese Journal of Ethnomedicine and Ethnopharmacy
基 金:国家自然科学基金(NO.:81303162);中国博士后科学基金(NO.:2015T80784;2014M552017);河南省博士后科研资助(NO.:2013010)
摘 要:目的:观察瑶药岗松根醇提物(BFTE)对大鼠佐剂性关节炎(AA)的药理作用。方法:42只大鼠随机分为正常组、模型组、雷公藤多苷组及BFTE高、中、低剂量组,完全弗氏佐剂诱导AA后,于第12天开始连续灌胃给药16d;同一时间点测定大鼠足趾肿胀度、关节炎评分、免疫器官指数;第29天处死大鼠,酶联免疫法(ELISA)测定大鼠血清中TNF-α、IL-6、IL-1β的含量,光学显微镜观察大鼠踝关节的病理变化。结果:与模型组相比,BFTE能够显著抑制AA大鼠的原发性和继发性足跖肿胀度,降低关节炎评分、免疫器官系数,改善大鼠踝关节病理状态,下调AA大鼠血清中炎症因子TNF-α、IL-6和IL-1β的水平。结论:BFTE对AA大鼠具有良好的治疗作用,其抗炎免疫的机理可能与减少TNF-α、IL-6和IL-1β的分泌有关。Objective To investigatethe pharmacological effects of Baeckea frutescens on adjuvant arthritis (AA) rats. Methods The 42 rats were randomly divided into six groups, including normal group, model group, positive control group (tripterygium glycosides), and high/medium/low dose groups oftotal extract of B. frutescens (BFFE). The complete Freund's adjuvant (CFA) -induced AA rats were used as model. After modeling, the intragastric administration began on the 12th day and last for 16 days, and the articular swell- ing, arthritis score, and immune organ index were measured during this time. The rats were sacrificed on the 29th day, and the inflam- matory factors of TNF-α、IL-6、IL-1β in the serum were detected by ELISA, and the pathological sections for ankle joints were made by hematoxylin- eosin (HE) staining. Results Compared with the model group, the BFTE could significantly inhibit the primary and secondary articular swelling, lower the arthritis score and immune organ index, improve the ankle pathologies, and reduce the serum levels of TNF-α、IL-6、IL-1β. Conclusion The roots of B. frutescens showed significant therapeutic effect on AA rats, and the anti - inflanunatory immunemeehanism may be related to decreasing the secretion of TNF-α、IL-6、IL-1β.
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