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目的研究三氧化二砷(As2O3)对Ⅱ型胶原诱导的关节炎(CIA)模型大鼠滑膜组织凋亡的影响,并进一步探讨As2O3对细胞因子肿瘤坏死因子(TNF)-α、白细胞介素(IL)-1的作用。方法将72只DA大鼠随机分成正常对照组、CIA大鼠模型组及不同浓度As2O3治疗组,共6组。As2O3治疗后第15天各组取膝关节滑膜、软骨和骨组织,光、电镜观察,TUNEL法检测凋亡。酶联免疫吸附试验(ELISA)测定血清细胞因子IL-1和TNF-α的浓度。结果治疗组滑膜组织病理改变比模型组减轻,滑膜细胞凋亡数明显增多,滑膜细胞超微结构接近正常对照组。并且与模型对照组相比,治疗组大鼠血清IL-1、TNF-α浓度降低,以第V组和第Ⅵ组更显著(P<0.01)。结论As2O3可能通过促进CIA大鼠滑膜细胞及组织的凋亡,抑制炎性因子TNF-α及IL-1的释放,起到减少CIA损害的保护作用。
Objective To investigate the effect of As2O3 on synovial tissue apoptosis induced by type Ⅱ collagen-induced arthritis (CIA) in rats and to further explore the effect of As2O3 on tumor necrosis factor (TNF) -α, interleukin (IL) -1 role. Methods Seventy-two DA rats were randomly divided into normal control group, CIA model group and As2O3 treatment group with 6 different concentrations. On the 15th day after As2O3 treatment, synovial, cartilage and bone tissues of knee joint were observed in each group. Light and electron microscopy were performed to observe apoptosis by TUNEL method. Serum levels of IL-1 and TNF-α were measured by enzyme-linked immunosorbent assay (ELISA). Results The pathological changes of synovial tissue in the treatment group were alleviated compared with the model group, the number of apoptosis of synovial cells increased significantly, and the ultrastructure of synovial cells was close to the normal control group. Compared with the model control group, the concentrations of IL-1 and TNF-α in serum of the treatment group decreased significantly, especially in the group V and the group VI (P <0.01). Conclusion As2O3 may play a protective role in reducing CIA injury by promoting apoptosis of synoviocytes and tissues of CIA rats and inhibiting the release of inflammatory cytokines TNF-α and IL-1.