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作 者:李晓红[1] 赵永娜[1] 邵晓霞[1] 李顺英[1] 张荣平[1]
机构地区:[1]昆明医学院药学院,昆明650031
出 处:《天然产物研究与开发》2008年第4期614-616,638,共4页Natural Product Research and Development
基 金:Science and Technology Foundation of Yunnan Education Administration
摘 要:观察滇产粗根荨麻水提取部分对佐剂性关节炎(adjuvant arthritis,AA)大鼠腹腔巨噬细胞(peritonealmacrophages,PMφ)分泌肿瘤坏死因子-α(tumor necrosis factor-alpha,TNF-α)及前列腺素E2(prostaglandin E2,PGE2)的影响。建立大鼠佐剂性关节炎模型,Ur水提取部分连续灌胃给药14或21 d后分次获取大鼠腹腔巨噬细胞,脂多糖(lipopolysaccharide,LPS)诱导大鼠腹腔巨噬细胞,用酶联免疫吸附法检测培养上清液中TNF-α及PGE2水平。AA大鼠腹腔巨噬细胞TNF-α及PGE2分泌较正常组升高,Ur水提取部分(400,200 mg/kg)对LPS诱导的AA大鼠腹腔巨噬细胞分泌TNF-α及PGE2水平有明显抑制作用。滇产粗根荨麻水提取部分对佐剂性关节炎的治疗作用可能与其抑制腹腔巨噬细胞分泌TNF-α及PGE2有关。To investigate the effects of aqueous fraction of Urtica macrorrhiza Hand-Mazz(Ur) on modulating tumor necrosis factor-alpha (TNF-α) and prostaglandin E2 (PGE2 ) production induced by lipopolysacchar/de (LPS) in peritoneal macrophages in adjuvant arthritis rats and elucidate the possible mechanisms of anti-inflammatory and antirheumatoid effects of Ur,adjuvant arthritis (AA) rat was used as the model. The PMφ samples were taken at different time after medication. TNF-α, PGE2 levels were measured by ELISA method. Production of TNF-α, and PGE2 increased in the culture supematant of PMφ in AA model rats. Ur(400 and 200 mg/kg) could inhibit TNF-α and PGE2 release induced by LPS from PMφ in AA rats. The anti-inflammatory mechanisms of Ur in AA rats might be related to its inhibitory effects on the level of TNF-α and PGE2 from PMφ in vivo.
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