摘要
目的:观察白芍总苷(TGP)对强直性脊柱炎(AS)的疗效和安全性及其对患者血清中IL-6、IL-10和TNF-α水平的影响,探讨TGP产生疗效的机制。方法:将98例AS患者随机分为两组,分别给予TGP和柳氮磺胺吡啶(SASP)联合双氯芬酸钠治疗,于治疗开始前和治疗后第1、12周进行临床疗效及安全性评估;并在治疗开始前及治疗12周后应用ELISA法测定血清IL-6、IL-10、TNF-α等细胞因子的水平。结果:两组治疗前和治疗12周后主要临床表现和病情活动性评价指标均无显著差异;两组治疗12周的疗效和总不良反应发生率亦无显著差异,但胃肠外不良反应的发生率TGP组为6.1%,SASP组为22.4%,以前者显著为低(P<0.05)。两组治疗前血清中IL-6、IL-10、TNF-α水平无显著差异,治疗12周后TGP组血清IL-10、TNF-α的水平显著低于SASP组(P均<0.05)。结论:TGP治疗AS疗效与SASP相近,但其胃肠道外的不良反应较少;TGP的疗效可能与其抑制患者血清中TNF-α等促炎性细胞因子有关。
To evaluate the efficacy and adverse reaction of total glucosides of paenoy (TGP,白芍总苷) in the treatment of ankylosing spondylitis (AS) and investigate the mechanism. Methods: Ninety-eight AS patients were randomly assigned to 2 groups. Patients of one group were treated with TGP and diclofenac sodium and those of the other group were treated with SASP and dielofenae sodium. Before treatment and at the end of the 12th week, clinic manifestation and disease activity index were observed and the serum levels of IL-6, IL-10 and TNF-α were determined using ELISA respeetively. Result: After 12 weeks of treatment, differences of major clinical manifestation, disease activity index, incidences of the efficacy and total adverse reaction between these two groups were not significant. Incidence of parenterally adverse reaetions in TGP group ( 6.1% ) was significantly lower than that in SASP group (22.4%) ( P 〈 0.05 ). Serum levels of IL-6, IL- 10 and TNF-α between two groups were not significant before treatment. But after 12 weeks, the serum level of IL-6 in TGP group was lower than that in SASP group (P 〈0.05 ) and so was the serum level of TNF-α( P 〈 0.05 ). Conclusion: Compared to SASP, TGP has the same efficacy but caused much less parenterally adverse reaction in the treatment of AS. The mechanism may be related to inhibition of IL-10 and TNF-α production.
出处
《中药药理与临床》
CAS
CSCD
北大核心
2009年第3期68-70,共3页
Pharmacology and Clinics of Chinese Materia Medica
关键词
白芍总苷
强直性脊柱炎
白细胞介素
肿瘤坏死因子-Α
Total glueosides of paenoy(白芍总苷)
ankylosing spondylitis ( AS )
interleukin
tumor necrosis factor-α