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期 刊 ：中国中药杂志 2005年 30卷 16期 页码：1296.

关键词：再生障碍性贫血；药物疗法；参麦注射液；肿瘤坏死因子α；CD34+细胞；细胞凋亡；

Keywords:chronic aplastic anemia, drug treatment, Shenmai injection, tumor necrosis factor-a, CE34+ cell, apoptosis,

摘 要 ：目的:探讨参麦注射液治疗慢性再生障碍性贫血(chronic aplastic anemia,CAA)的疗效及其作用机制。方法:将65例CAA患者随机分为治疗组和对照组,治疗组采用参麦注射液配合西药常规治疗,对照组单用西药治疗,治疗后进行疗效评价,并分别于治疗前后检测患者血清肿瘤坏死因子(tumornecrosisfactor-α,TNF-α)水平,以及采用免疫磁珠分离系统(MACS)分离纯化骨髓CD₃₄⁺细胞,用DNA末端原位标记(TUNEL)技术分析骨髓CD₃₄⁺细胞原位凋亡状况。结果:治疗组总有效率为63.6%,对照组总有效率为40.6%,治疗组疗效明显优于对照组(P<0.01);治疗前,CAA患者血清TNF-α浓度、骨髓CD₃₄⁺细胞凋亡率均明显高于健康对照组(P<0.01),治疗后,治疗组血清TNF-α浓度明显降低(P<0.01),骨髓CD₃₄⁺细胞凋亡率减低(P<0.05),与对照组相比均有显著差异(P<0.05)。结论:参麦注射液治疗CAA疗效确切,其机制可能为降低CAA患者血清TNE-α浓度,减少骨髓CD₃₄⁺细胞凋亡。

Abstract:Objective: To investigate the effect of Shenmai injection on chronic aplastic anemia patients and its mechanism. Method: Sixty-five chronic aplastic anemia patients were randomized into treatment group and control group. The patients of the treatment group were treated by injecting Shenmai injection and taking western medicine orally, those of the control group taking western medicine orafly only, then the effect was evaluated. The concentration of tumor necrosis factor-α(TNF-α) in blood serum was detected and the apoptosis of bone marrow CD₃₄⁺ cell was analysed by DNA ISEL technic before and after treatment. Result: The effective rate of the treatment group and the control group was 63.6 % and 40.6 % respectively, the effect of the Shenmai injection on the treatment group was obviously better than that of the control group (P<0.01). Before treatment, the concentration of TNF-α in blood serum and the apoptosis rate of bone marrow CD₃₄⁺ cell of the chronic aplastic anemia patient were higher than normal (P< 0.01). After treatment, the concentration of TNF-a in blood serum of the treatment group decreased obviously(P< 0.01), and the apoptosis rate of bone marrow CD₃₄⁺ cell of the treatment group also decreased (P< 0.05), which had significant difference compared with those of the control group(P< 0.05). Conclusion: Shenmai injection is efficient to chronic aplastic anemia. The mechanism is decreasing the concentration of TNF-a in blood serum and the apoptosis rate of bone marrow CD₃₄⁺ cell.

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