雷公藤治疗对艾滋病患者CD4^+T淋巴细胞及炎症因子水平的影响

Effect of Tripterygium Wilfordii treatment on CD4^+T lymphocyte and inflammatory factors in AIDS patients

目的:探究雷公藤治疗对艾滋病(AIDS)患者CD4^+T淋巴细胞及炎症因子水平的影响。方法:选择符合入选标准的患者68例,随机分配为对照组和观察组,每组各34例。对照组采用HAART治疗,观察组在对照组基础上予以雷公藤治疗,比较两组治疗前及治疗6个月及12个月后CD4+细胞计数、IFN-γ、TNF-ɑ及IP-10的变化情况及免疫重建有效率。结果:治疗后,两组CD4^+T细胞数量随治疗时间延长呈上升趋势,较治疗前增加(P <0. 05);两组炎症因子随治疗时间呈下降趋势。观察组在治疗6及12个月的CD4^+T细胞数量均高于对照组,但差异无统计学意义(P> 0. 05),其炎症因子水平低于对照组及治疗前(P <0. 05)。观察组治疗后其免疫重建总有效率高于对照组(P <0. 05)。结论:雷公藤联合HAART治疗可有效提高AIDS患者免疫重建有效率,其作用机制可能与增加CD4^+T细胞数量及降低炎症因子水平有关。

Objective： To explore the effect of Tripterygium Wilfordii treatment on CD4 ＋T lymphocyte and inflammatory factors in AIDS patients. Methods： 68 patients who met the inclusion criteria were randomly allocated to the control group and the observation group,34 cases in each group.The control group was treated with HAART only.The observation group was treated with Tripterygium Wilfordii on the basis of the control group.The changes of CD4 ＋ cell count,IFN-γ,TNF-ɑ,IP-10 and the immune reconstruction efficiency were compared between the two groups at before and 6 months and 12 months after treatment. Results： After treatment,the number of CD4 ＋T cells in the two groups showed an upward trend with the extension of treatment time,which increased significantly compared with those before treatment （ P 〈0.05）.The two groups of inflammatory factors decreased with the time of treatment.The number of CD4 ＋T cells in the observation group at 6 and 12 months after treatment was higher than that in the control group （ P 〉0.05）,but the difference was not significant （ P 〈0.05）.The level of inflammatory factors was lower than that in the control group and before treatment （ P 〈0.05）.After treatment,the total effective rate of immune reconstitution in observation group was significantly higher than that in control group and before treatment （ P 〈0.05）. Conclusion： Tripterygium wilfordii combined with HAART can effectively improve the efficiency of immune reconstruction in AIDS patients,and its mechanism may be related to increasing the number of CD4 ＋T cells and reducing the level of inflammatory factors.