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目的:观察佐剂关节炎(adjuvant arthritis,AA)大鼠ApoA1、HDL和VEGF、E选择素及血管内皮超微结构的变化及新风胶囊(XFC)对其的影响。方法:用弗氏完全佐剂(Freund′scompleteadjuvant,CFA)诱发大鼠产生关节炎,观察AA大鼠ApoA1、HDL、VEGF、E选择素、细胞因子、关节肿胀度、关节炎指数(arthritisindex,AI)及血管内皮超微结构的变化以及XFC对其的影响,并进行相关性分析。结果:AA大鼠ApoA1、HDL差异率的变化:模型组ApoA1、HDL升高率明显高于正常组、XFC组、MTX组(P<0.05),与TPT组无显著差异(P>0.05)。XFC能下调AA大鼠ApoA1、HDL的表达(P<0.05)。XFC组与正常对照组无显著差异(P>0.05)。AA大鼠VEGF、E选择素及IL-1β、IL-10、CRP的变化:与模型对照组相比,正常组、XFC组VEGF、E选择素、IL-1β、CRP显著降低(P<0.01或P<0.05),IL-10显著升高;XFC能显著下调AA大鼠VEGF、E选择素、IL-1β、CRP的表达,上调IL-10的表达。AA大鼠血管超微结构的变化:与正常对照组相比:模型组、XFC、甲氨喋呤(MTX)、雷公藤多苷片(TPT)组血管内皮超微结构均出现不同程度破坏:与模型对照组相比:XFC、甲氨喋呤(MTX)、雷公藤多苷片(TPT)组血管内皮超微结构改善明显,XFC组改善明显优于TPT组、MTX组。XFC对AA大鼠足跖肿胀度、关节炎指数的影响:与模型对照组相比,XFC、甲氨喋呤(MTX)、雷公藤多苷片(TPT)组肿胀度均明显下降(P<0.05),与正常对照组相比无明显差异(P>0.05);与模型对照组相比,各组AA大鼠的关节炎指数均显著降低(P<0.05),XFC组与TPT组相比无明显差异(P<0.05)。AA大鼠ApoA1、HDL与足跖肿胀度、关节炎指数、VEGF、E选择素及细胞因子的相关分析:模型对照组ApoA1、HDL与VEGF、E选择素、IL-1β呈显著负相关(P<0.05或P<0.01),与足跖肿胀度、关节炎指数、CRP呈显著正相关(P<0.05或P<0.01),与IL-10无明显相关。结论:免疫应激引起AA大鼠ApoA1、HDL的改变,AA大鼠ApoA1、HDL的改变与疾病的活动度、细胞因子的紊乱、血管内皮的损伤相关,ApoA1、HDL参与了血管内皮损伤的过程,XFC可下调ApoA1、HDL的表达及改善血管内皮的损伤,明显优与MTX组与TPT组。其机制可能是通过调节细胞因子间接下调ApoA1、HDL改善血管内皮的损伤。
OBJECTIVE: To observe the changes of ApoA1, HDL and VEGF, E-selectin, and the ultrastructure of vascular endothelium in rats with adjuvant arthritis (AA) and the effects of Xinfeng capsule (XFC) on them. METHODS: Arthritis was induced in rats with Freund’s complete adjuvant (CFA). The ApoA1, HDL, VEGF, E-selectin, cytokines, joint swelling, and arthritis index (AI) were observed in AA rats. Changes in the ultrastructure of the vascular endothelium and the effects of XFC on it, and correlation analysis. RESULTS: The ApoA1 and HDL variability in AA rats were significantly higher in the model group than in the normal group, XFC group, and MTX group (P<0.05), but not significantly different from the TPT group (P>0.05). XFC could down-regulate the expression of ApoA1 and HDL in AA rats (P<0.05). There was no significant difference between the XFC group and the normal control group (P>0.05). Changes of VEGF, E-selectin and IL-1β, IL-10 and CRP in AA rats: VEGF, E-selectin, IL-1β and CRP were significantly decreased in normal and XFC groups compared with the model control group (P<0.01). Or P<0.05), IL-10 was significantly increased; XFC could significantly down-regulate the expression of VEGF, E-selectin, IL-1β, CRP and up-regulate the expression of IL-10 in AA rats. Changes in vascular ultrastructure of AA rats: Compared with the normal control group, the ultrastructure of the vascular endothelium in the model group, XFC, methotrexate (MTX), triptolide polypivoxil (TPT) groups were destroyed in varying degrees: Compared with the model control group, the ultrastructure of the vascular endothelium was significantly improved in the XFC, methotrexate (MTX), and triptolide (TPT) groups, and the XFC group was significantly better than the TPT group and the MTX group. The effect of XFC on foot swelling and arthritis index in AA rats:Compared with the model control group, the degree of swelling in XFC, MTX, and Triptolide Tablets (TPT) group was significantly decreased (P< 0.05), compared with the normal control group, there was no significant difference (P> 0.05); compared with the model control group, the arthritis index of each group of AA rats was significantly reduced (P <0.05), XFC group compared with the TPT group No significant difference (P<0.05). Correlation analysis of ApoA1, HDL, swelling degree of arthritis, arthritis index, VEGF, E-selectin and cytokines in AA rats: Model control group ApoA1, HDL and VEGF, E-selectin, IL-1β were significantly negatively correlated (P (<0.05 or P<0.01). There was a significant positive correlation with paw swelling, arthritis index and CRP (P<0.05 or P<0.01). There was no significant correlation with IL-10. CONCLUSION: Immune stress induces the changes of ApoA1 and HDL in AA rats. The changes of ApoA1 and HDL in AA rats are associated with the degree of disease activity, disorders of cytokines and damage of vascular endothelium. ApoA1 and HDL participate in the process of vascular endothelial injury. XFC can down-regulate the expression of ApoA1, HDL and improve the damage of vascular endothelium, and it is obviously superior to MTX group and TPT group. The mechanism may be through the regulation of cytokines indirectly down-regulated ApoA1, HDL improve vascular endothelial damage.