摘要
目的观察历节胶囊对CIA小鼠TLR4/MyD88/NF-κB信号通路的影响,探讨其治疗类风湿关节炎(RA)的作用机制。方法将60只DBA/1小鼠随机分成3组:正常组,模型组,历节胶囊组,每组各20只。每组给药连灌21天后处死。Western blot检测TLR4、MyD88、NF-κB p65蛋白表达量;PCR检测TLR4、MyD88、NF-κB p65的mRNA表达水平;ELISA检测血清肿瘤坏死因子-α(TNF-α)水平。结果与正常组比较,模型组MyD88、NF-κB p65及TLR4的mRNA及蛋白表达量均上升,模型组的血清TNF-α水平升高,差异均有统计学意义(P<0.01或P<0.05)。与模型组比较,历节胶囊组MyD88、NF-κB p65及TLR4 mRNA及蛋白表达量均下降,血清TNF-α水平下降,差异均有统计学意义(P<0.05)。结论历节胶囊可以通过抑制TLR4/MyD88/NF-κB p65炎症信号通路以取得疗效。
Objective To observe the effect of Lijie Capsule on TLR4/MyD88/NF-κB signaling pathway in CIA mice,and to explore its mechanism of action in the treatment of RA.Methods 60 DBA/1 mice were RAndomly divided into 3 groups:normal group,model group and treatment group,with 20 mice in each group.Each group was sacrificed after 21 days of continuous perfu-sion.Western blot was used to detect the protein expressions of TLR4,MyD88 and NF-κB p65;PCR was to detect the mRNA expression levels of TLR4,MyD88 and NF-κB p65;ELISA was to detect the level of serum tumor necrosis factor-α(TNF-α).Results Compared with the normal group,the mRNA and protein expressions of MyD88,NF-κB p65 and TLR4 in the mod-el group were increased,and the serum TNF-αlevel in the model group was increased,and the differences were statistically sig-nificant(P<0.01 or P<0.05).Compared with the model group,the mRNA and protein expressions of MyD88,NF-κB p65 and TLR4 in the treatment group decreased,and the level of serum TNF-αdecreased,with statistical significance(P<0.05).Conclusion Lijie Capsule can be effective by inhibiting TLR4/MyD88/NF-κB p65 inflammatory signaling pathway.
作者
杨灵梅
甘丽贤
黄秉慧
覃文瑜
陈延强
YANG Ling-mei;GAN Li-xian;HUANG Bing-hui;QIN Wen-yu;CHEN Yan-qiang(Guangxi University of Chinese Medicine,Nanning,530001,China;First Affiliated Hospital of Guangxi University of Chinese Medicine,Nanning,530022,China)
出处
《时珍国医国药》
CAS
CSCD
北大核心
2023年第9期2095-2098,共4页
Lishizhen Medicine and Materia Medica Research
基金
国家自然科学基金(81860825)。
关键词
历节胶囊
类风湿关节炎
炎症通路
脾为之卫
TOLL样受体
Lijie Capsule
Rheumatoid arthritis
Inflammatory pathway
Theory of"spleen as the defense of zang-fu viscera"
Toll-like receptor