CAJ | 학술논문

目的：探讨青藤碱对佐剂性关节炎大鼠Toll样受体（TLR）2mRNA及MyD88mRNA表达的影响。方法清洁级SD大鼠40只，随机分为模型组、青藤碱组、甲氨蝶呤组及正常对照组。前3组大鼠右后足跖皮内注射弗氏完全佐剂诱发大鼠佐剂性关节炎模型，正常对照组大鼠右后足跖皮内注射等量0.9％氯化钠注射液。各组分别干预4周后，取膝关节滑膜，采用实时聚合酶链反应（PCR）法检测TLR2mRNA，MyD88mRNA表达，酶联免疫吸附试验（ELISA）法检测肿瘤坏死因子（TNF）-α。结果模型组大鼠膝关节滑膜组织TLR2mRNA，MyD88mRNA表达及TNF-α均较正常对照组明显升高，差异有统计学意义（均为P＜0．01）。经青藤碱治疗后，TLR2mRNA，MyD88mRNA表达及TNF-α均较模型组明显下降，差异有统计学意义（均为P＜0．01）。结论青藤碱可改善佐剂性关节炎大鼠的关节炎症，该作用可能与抑制TLR2通路有关。
목적：탐토청등감대좌제성관절염대서Toll양수체（TLR）2mRNA급MyD88mRNA표체적영향。방법청길급SD대서40지，수궤분위모형조、청등감조、갑안접령조급정상대조조。전3조대서우후족척피내주사불씨완전좌제유발대서좌제성관절염모형，정상대조조대서우후족척피내주사등량0.9％록화납주사액。각조분별간예4주후，취슬관절활막，채용실시취합매련반응（PCR）법검측TLR2mRNA，MyD88mRNA표체，매련면역흡부시험（ELISA）법검측종류배사인자（TNF）-α。결과모형조대서슬관절활막조직TLR2mRNA，MyD88mRNA표체급TNF-α균교정상대조조명현승고，차이유통계학의의（균위P＜0．01）。경청등감치료후，TLR2mRNA，MyD88mRNA표체급TNF-α균교모형조명현하강，차이유통계학의의（균위P＜0．01）。결론청등감가개선좌제성관절염대서적관절염증，해작용가능여억제TLR2통로유관。
Objective To investigate the effects of sinomenine on the expression of TLR2 mRNA and MyD88 mRNA in rats with adjuvant arthritis .Methods Forty SD rats were randomly divided into model group , sinomenine group ,methotrexate group and normal control group .Rats from the first three groups were induced rat model of adjuvant arthritis by intradermal injection of Freund′s in right paw ,and rats from the normal control group were injected saline .After the rats from different groups were treated for four weeks respectively ,the rats knee synovium were taken out to detect the expression of TLR2 mRNA and MyD88 mRNA using real-time PCR method ,and the expression of inflammatory cytokines TNF-α by ELISA.Results The expression of TLR2 mR-NA ,MyD88 mRNA and TNF-αof synovial tissue in the model rats significantly higher than those in the normal control group .The difference was statistically significant (all P<0 .01) .After treated by sinomenine ,the expres-sion of TLR2mRNA ,MyD88 mRNA and TNF-αof synovial tissue significantly decreased compared with the mod-el rats ,and the difference was statistically significant (all P<0 .01) .Conclusion Sinomenine can improve arthritis in rats with adjuvant arthritis ,which may be related to inhibition of TLR2 signaling pathway.