那如-3对胶原诱导性关节炎大鼠的保护作用

Protective effect of Naru-3 on collagen-induced arthritis in rats

目的基于影像学方法探讨蒙药那如-3对类风湿关节炎大鼠的保护作用。方法将大鼠分为正常组、模型组、阳性组及那如-3低、中、高剂量组(0.1、0.2、0.4 g/kg),采用免疫诱导法构建胶原诱导性关节炎(CIA)大鼠模型,给药4周后,观察各组大鼠关节炎评分(AI)及体质量变化。采用ELISA法检测各组大鼠血清VEGF、TNF-α及IL-1水平,高频超声及超声造影(CEUS)评估滑膜增生及新生血管情况,X射线及高分辨率显微计算机断层扫描(micro-CT)评估踝关节骨质破坏情况,HE及免疫组化法观察关节滑膜结构及CD31、VEGF、TNF-α、IL-1β表达。结果与模型组比较,那如-3各剂量组大鼠体质量增加(P<0.05),AI评分未见明显变化(P>0.05),血清VEGF、TNF-α水平、滑膜厚度、能量多普勒成像(PDI)血流分级及造影强度、X射线评分、CD31表达均降低(P<0.05),高剂量组IL-1水平及HE评分均降低(P<0.05)。结论那如-3对类风湿关节炎大鼠关节组织具有保护作用,其可能通过抑制滑膜新生血管及炎性细胞因子减轻滑膜炎症,减轻骨侵蚀,延缓病情进展。

AIM To investigate the protective effect of Mongolian medicine Naru-3 on rat rheumatoid arthritis(RA)using imaging method.METHODS With the rats divided into the normal group,the model group,the positive medicine group,and the low,medium and high dose Naru-3 groups(0.1,0.2 and 0.4 g/kg),the rat model of collagen-induced arthritis(CIA)was established by immune induction method.After 4 weeks of corresponding drug administration,the rats had their changes of arthritis index(AI)level and body weight observed;their serum levels of VEGF,TNF-α and IL-1 detected by ELISA;their synovial hyperplasia and neovascularization evaluated by high-frequency ultrasound and contrast-enhanced ultrasound(CEUS);their bone destruction of ankle joint evaluated by X-ray and high-resolution micro-CT;and their synovial membrane and expressions of CD31,VEGF,TNF-α and IL-1β observed by HE and immunohistochemistry.RESULTS Compared with the model group,the Naru-3 groups displayed increased rat weight(P<0.05);no significantly changed AI score(P>0.05);and overally decreased levels of serum VEGF,TNF-α,synovial membrane thickness,blood flow signal by power Doppler imaging(PDI)and contrast intensity revealed,X-ray score,and CD31 expression(P<0.05),in addition to the decreased level of IL-1 and HE score in high-dose group(P<0.05).CONCLUSION Naru-3 is protective to the joint tissue in rat model of RA through alleviating synovitis,bone erosion and delaying the progress of the disease by inhibiting synovial neovascularization and inflammatory cytokines.