CAJ | 학술논문

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。
목적：탐토고행인감대Ⅱ형효원유도성관절염(CIA)대서적항염작용궤제。방법 Wistar대서수궤분위정상조、모형조、고행인감조、뢰공등다감조。채용Ⅱ형효원유도건립CIA대서모형，조모후제15일，각급약조여상응약물관위，련속28 d。ELISA검측대서혈청종류배사인자-α(TNF-α)、세포간점부분자-1(sICAM-1)수평，면역조화법검측대서관절활막TNF-α표체。결과고행인감조화뢰공등다감조관절활막TNF-α양성표체상사，교모형조명현감소，차고행인감조화뢰공등다감조대서외주혈중TNF-α、sICAM-1수평여모형조비교균명현하강(P＜0.05)，여정상조비교차이무통계학의의(P＞0.05)。결론고행인감통과유효억제TNF-α、sICAM-1수평급TNF-α표체，체도치료류풍습관절염적작용。
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.