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作 者:万强[1] 裴正学[1] 江秀娟[1] 郭红云[2] 李德杏[2] 梁涛[2] 张永东[2] 李雪萍[2] 胡清荣[2] 高波[2]
机构地区:[1]甘肃省肿瘤医院,甘肃兰州730050 [2]甘肃省医学科学研究院,甘肃兰州730050
出 处:《中国中医药信息杂志》2012年第1期45-46,49,共3页Chinese Journal of Information on Traditional Chinese Medicine
基 金:甘肃省中医药管理局资助项目(2005-GKS-10)
摘 要:目的通过观察消风Ⅱ号胶囊对佐剂性关节炎(AA)大鼠炎性组织中前列腺素E2(PGE2)及一氧化氮(NO)含量的影响,探讨其治疗类风湿关节炎作用机理。方法将AA大鼠随机分为模型组及消风Ⅱ号胶囊低(188 mg/kg)、高剂量组(375 mg/kg),同时设正常组。致炎第7日开始灌胃给予药物,灌胃剂量为1.0 mL/100 g体质量,模型组给予等体积的蒸馏水,连续21 d。给药结束后次日处死大鼠,测量AA大鼠炎性组织中PGE2及NO含量。结果消风Ⅱ号胶囊低、高剂量组均可抑制大鼠非佐剂注射侧炎性组织中PGE2的生物合成,抑制率分别为41.2%和33.6%,抑制大鼠佐剂注射侧炎性组织中NO含量,抑制率分别为39.9%和29.7%,与模型组相比,差异有统计学意义(P<0.001,P<0.01)。结论消风Ⅱ号胶囊抗关节炎作用通过抑制PGE2和NO的合成或释放,使局部炎性组织中PGE2及NO含量下降而发挥作用。Objective To investigate the mechanism of Xiaofeng Ⅱ capsule for rheumatoid arthritis by studying the effect of Xiaofeng Ⅱ capsule on PGE2 and NO content of inflammatory organization in adjuvant arthritis (AA) rats. Methods AA rats were divided randomly into model group, low-dosage (188 mg/kg) of Xiaofeng Ⅱ capsule group (low-dosage group), high-dosage (375 mg/kg) of Xiaofeng Ⅱ capsule group (high-dosage group) and normal group. After inducing inflammation, AA rats were gastric perfused on the seventh day with Xiaofeng Ⅱ capsule of 1.0 mL/100 g, and with distilled water of equal volume in model group, continuously for 21 days. Executed the rats to measuring PGE2 and NO content of inflammatory organization in AA rats the second day after the last medication. Results Either low-dosage group or high-dosage group could restrain PGE2 biosynthesis of inflammatory organization in the side of injected adjuvant, the inhibition rate was 41.2% and 33.6% respectively. The two groups could restrain NO content of inflammatory organization in the side not injected adjuvant, the inhibition rate was 39.9% and 29.7% respectively. Compared with model group, differences had statistical significance (P〈0.001, P〈0.01). Conclusion The mechanism of Xiaofeng Ⅱ capsule for arthritis is that it can reduce PGE2 and NO content of local inflammatory organization by restraining the biosynthesis of PGE2 and NO or restraining the release of them.
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