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目的探讨沙利度胺对胶原诱导性关节炎(collagen-induced arthritis,CIA)大鼠红系祖细胞的影响机制。方法40只雄性Wistar大鼠随机分为正常对照组、模型组、高、低剂量沙利度胺组和甲氨喋呤组,制定CIA大鼠模型,于初次免疫后第12 d给药,第21 d及第60 d处死大鼠,测定甲基纤维素半固体培养基中大鼠骨髓红系集落数目;流式细胞术测定骨髓单个核细胞中的CD34+/CD71+细胞数目并应用7-氨基放线菌D(7-amino-actinomycin D,7AAD)染色检测其凋亡率;ELISA法测定大鼠血清肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)的浓度。结果模型组大鼠骨髓红系形成集落的能力明显下降(P<0.05);骨髓CD34+/CD71+细胞数目减少(P<0.05),且凋亡率明显增加(P<0.05);血清中TNF-α浓度明显增加(P<0.05)。沙利度胺可以提高模型组大鼠骨髓红系集落及CD34+/CD71+细胞的数目(P<0.05),降低后者的凋亡率及血清TNF-α水平(P<0.05)。结论胶原诱导性关节炎大鼠骨髓红系祖细胞的凋亡明显增加,沙利度胺可以减少凋亡率,增加骨髓红系造血。
Objective To investigate the effect of thalidomide on erythroid progenitor cells in collagen-induced arthritis (CIA) rats. Methods Forty male Wistar rats were randomly divided into normal control group, model group, high and low dose thalidomide group and methotrexate group. CIA rat model was established and administered on the 12th day after the first immunization. The rats were sacrificed on day 21 and day 60, and the numbers of bone marrow erythroid colonies in methylcellulose semi-solid medium were determined. The number of CD34 + / CD71 + cells in bone marrow mononuclear cells was determined by flow cytometry and the number of CD34 + / CD71 + The apoptotic rate was detected by staining with 7-amino-actinomycin D (7AAD). The concentration of tumor necrosis factor-α (TNF-α) in serum was determined by ELISA. Results The number of CD34 + / CD71 + cells in the bone marrow decreased significantly (P <0.05), and the apoptosis rate was significantly increased (P <0.05). The level of TNF-α Concentration significantly increased (P <0.05). Thalidomide could increase the number of erythroid colony and CD34 + / CD71 + cells in the model group (P <0.05), decrease the latter’s apoptosis rate and serum TNF-α level (P <0.05). Conclusion The apoptosis of myeloid erythroid progenitor cells in collagen-induced arthritis rats was significantly increased. Thalidomide could reduce the apoptosis rate and increase the hematopoietic potential of myeloid erythrocytes.