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目的:研究彝族药汝无糯鸡对佐剂性关节炎(AA)大鼠模型的滑膜病变及滑膜细胞核转录因子-κB(NF-κB),基质金属蛋白酶-2(MMP-2)和MMP-9表达的影响,探讨其抗类风湿性关节炎(RA)的作用机制。方法:60只SD大鼠随机分成空白组,模型组,尼美舒利组,汝无糯鸡高、中、低剂量组(按生药量计5.0,2.5,1.25 g·kg-1),采用完全弗氏佐剂建立AA大鼠模型,灌胃给药28 d后取样并处死大鼠,苏木素-伊红(HE)染色光镜下观察大鼠踝关节滑膜组织形态学变化,酶联免疫吸附法(ELISA)测定大鼠血清白细胞介素(IL)-1β,IL-6,IL-10,肿瘤坏死因子-α(TNF-α),一氧化氮(NO),前列腺素E2(PGE2)含量,免疫组化法检测大鼠滑膜组织中NF-κB,MMP-2,MMP-9的表达水平。结果:彝族药汝无糯鸡组明显减轻滑膜细胞的异常增殖,减少炎性细胞浸润,各剂量组不同程度降低AA大鼠血清中IL-1β,IL-6,TNF-α,NO,PGE2的含量和升高IL-10的含量,降低关节滑膜组织NF-κB,MMP-2,MMP-9的蛋白含量(P<0.05,P<0.01)。结论:彝族药汝无糯鸡治疗RA的作用机制可能是通过下调AA大鼠滑膜组织中NF-κB,MMP-2,MMP-9的蛋白表达,抑制炎性细胞因子生成,从而加速细胞凋亡,改善滑膜病变。
Objective: To investigate the synovial pathological changes and the expressions of NF-κB, MMP-2 and MMP-2 in synovial cells of adjuvant arthritis (AA) MMP-9 expression, explore its anti-rheumatoid arthritis (RA) mechanism of action. Methods: Sixty Sprague-Dawley rats were randomly divided into three groups: blank group, model group, nimesulide group, Ruyouluo chicken high, medium and low dose groups (5.0,2.5,1.25 g · kg-1) The rat model of AA was established by complete Freund’s adjuvant. The rats were sacrificed 28 days after intragastric administration, and the morphological changes of ankle synovium were observed under hematoxylin-eosin (HE) staining. The levels of serum interleukin (IL) -1β, IL-6, IL-10, TNF-α, NO and PGE2 were determined by enzyme-linked immunosorbent assay (ELISA) Content, immunohistochemistry of rat synovial tissue NF-κB, MMP-2, MMP-9 expression levels. Results: The YiRuYuWuNuoNuo group significantly reduced synovial cell proliferation and decreased inflammatory cell infiltration. The levels of IL-1β, IL-6, TNF-α, NO, PGE2 (P <0.05, P <0.01) .Conclusion: The content of IL-10 and the content of IL-10 in synovial tissue of rats with synovial membrane and the content of NF-κB, MMP- CONCLUSION: The mechanism of RA YiRuyou no waxy chicken may be through down-regulating the protein expression of NF-κB, MMP-2 and MMP-9 in synovial tissue of AA rats, inhibiting the production of inflammatory cytokines and accelerating the apoptosis of RA Death, improve synovial lesions.