苦杏仁苷对Ⅱ型胶原诱导性关节炎大鼠肿瘤坏死因子-α和细胞间黏附分子-1的影响  

Effects of Amygdalin on TNF-α and sICAM-1 of Rats with Type Ⅱ Collagen-induced Arthritis

作　　者：罗德梅[1] 单志桂[1] 葛金莲[1] 刘青[1] 罗莉[1] 

机构地区：[1]新疆医科大学第一附属医院,新疆乌鲁木齐830011

出　　处：《中国中医药信息杂志》2015年第7期75-77,共3页Chinese Journal of Information on Traditional Chinese Medicine

基　　金：新疆维吾尔自治区自然科学基金(2014211C047);新疆医科大学第一附属医院药学专项基金(2012YX06)

摘　　要：目的探讨苦杏仁苷对Ⅱ型胶原诱导性关节炎(CIA)大鼠的抗炎作用机制。方法 Wistar大鼠随机分为正常组、模型组、苦杏仁苷组、雷公藤多苷组。采用Ⅱ型胶原诱导建立CIA大鼠模型,造模后第15日,各给药组予相应药物灌胃,连续28 d。ELISA检测大鼠血清肿瘤坏死因子-α(TNF-α)、细胞间黏附分子-1(sICAM-1)水平,免疫组化法检测大鼠关节滑膜TNF-α表达。结果苦杏仁苷组和雷公藤多苷组关节滑膜TNF-α阳性表达相似,较模型组明显减少,且苦杏仁苷组和雷公藤多苷组大鼠外周血中TNF-α、sICAM-1水平与模型组比较均明显下降(P<0.05),与正常组比较差异无统计学意义(P>0.05)。结论苦杏仁苷通过有效抑制TNF-α、sICAM-1水平及TNF-α表达,达到治疗类风湿关节炎的作用。Objective To discuss effects of anti-inflammatory mechanism of amygdalin on rats with type II collagen-induced arthritis （CIA）. Methods Wistar rats were randomized into normal group, model group, amygdalin group, and tripterygium group. Type II CIA rat models were established. From the 15th day after the modeling establishment, each administration group was given corresponding dose of medicine for continuous 28 days. Levels of TNF-αand sICAM-1 were detected by ELISA in serum of rats, and expression of TNF-α was detected by immuno-histochemical method. Results TNF-α positive expression in amygdalin group and tripterygium group was similar and significantly reduced compared with model group. Levels TNF-α and sICAM-1 in amygdalin group and tripterygium group significantly decreased compared with those in model group （P〈0.05）, without significant difference compared with normal group （P〈0.05）. Conclusion Amygdalin can inhibit the expression of TNF-α and levels of TNF-α and sICAM-1, in order to treat rheumatoid arthritis.

关 键 词：苦杏仁苷 Ⅱ型胶原诱导性关节炎 肿瘤坏死因子-Α 细胞间黏附分子-1 大鼠 

分 类 号：R285.5[医药卫生—中药学]