青藤碱对佐剂性关节炎大鼠TLR4/MyD88信号通路的影响

Effect of Sinomenine on the TLR4/MyD88 signal pathway in rats with adjuvant arthritis

目的:探讨青藤碱对佐剂性关节炎大鼠TLR4/My D88信号通路诱导炎症的影响。方法:选择清洁级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。4组分别干预4周后,取膝关节滑膜,采用Real-time PCR法检测TLR4 m RNA、My D88 m RNA表达,ELISA法检测炎性因子TNF-α。结果:模型组大鼠膝关节滑膜组织TLR4 m RNA、My D88m RNA及炎性因子TNF-α表达均较正常对照组明显升高(P<0.01)。经青藤碱治疗后,TLR4 m RNA、My D88 m RNA及炎性因子TNF-α表达均较模型组明显下降(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TLR4/My D88信号通路有关。

Objective：To investigate the effects of Sinomenine on TLR4/MyD88 signal pathway in rats with adjuvant arthritis. Methods：Forty SD rats were randomly divided into the model group,Sinomenine group,methotrexate group and normal control group. The rat model of adjuvant arthritis in first three groups were induced by intradermal injecting Freund＇s into right paw,the normal control group were injected with saline. The mRNA expressions of TLR4 and MyD88 and level of TNF-αin knee synovium of four groups were detected by real-time PCR and ELISA after 4 weeks of intervention, respectively. Results：The levels of TLR4 and MyD88 mRNA expressions,and TNF-α of synovial tissue in model rats were significantly higher than those in normal control group（P 〈0. 01）. Compared with the model rats, the levels of TLR4 and MyD88 mRNA expressions, and TNF-α significantly were decreased after treatment with Sinomenine（P〈0. 01）. Conclusions：Sinomenine can improve the adjuvant arthritis in rats,which may be by inhibiting the TLR4/MyD88 signal pathway.