电针足三里、宣中对佐剂性关节炎大鼠滑膜血管生成的影响。

Jiang Jianzhen, Zhang Xin, Luo Zhenguo, S U Chengguo, Zhou Haiyan, Jiang Yuqing, Xiao Xianjun, Chen Yunfei, Zhu Jun
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引用次数: 0

摘要

目的:观察电针足三里、宣中对佐剂性关节炎(AA)大鼠滑膜血管生成的影响。方法:雄性Sprague-Dawley大鼠双侧注射弗氏完全佐剂(FCA)建立AA模型。注射后3天,在足三里(ST36)和玄中(GB39)穴位给大鼠电针,每隔一天一次,持续16d。对每只动物进行关节炎指数评分、爪体积和苏木精-伊红(HE)染色。观察滑膜组织中血管生成标志物分化簇34(CD34)的表达和滑膜细胞凋亡。随后检测Notch1、毛状和分裂同源物增强因子-1(Hes1)、转化生长因子β(TGF-β)和碱性成纤维细胞生长因子(bFGF)的水平。结果:电针能显著降低关节炎指数、爪体积和HE染色评分。电针能显著抑制AA大鼠关节滑膜组织CD34的表达,促进滑膜细胞凋亡。电针治疗显著下调Notch1信号通路蛋白和mRNA(Notch1、Hes1、TGF-β和bFGF)的表达。结论:这些结果证明EA通过抑制AA大鼠模型中的Notch1信号通路来减弱滑膜血管生成。基于我们的发现,我们提出电针是一种很有前途的类风湿性关节炎的补充和替代疗法。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Efficacy of electroacupuncture stimulating Zusanli (ST36) and Xuanzhong (GB39) on synovial angiogenesis in rats with adjuvant arthritis.

Objective: To investigate the efficacy of electroacupuncture (EA) stimulating Zusanli (ST36) and Xuanzhong (GB39) on synovial angiogenesis in rats with adjuvant arthritis (AA).

Methods: AA models were established by bilateral injection of Freund's complete adjuvant (FCA) in male Sprague-Dawley rats. Three days after injection, rats were given EA at Zusanli (ST36) and Xuanzhong (GB39) acupoints, once every other day, for 16 d. The arthritis index score, paw volume, and hematoxylin-eosin (HE) staining was performed for each animal. Angiogenesis marker cluster of differentiation 34 (CD34) expression and synovial cell apoptosis in synovial tissue were observed. The levels of Notch1, hairy and enhancer of split homolog-1 (Hes1), transforming growth factor-beta (TGF-β) and basic fibroblast growth factor (bFGF) were subsequently detected.

Results: We found that EA significantly decreased arthritis index scores, paw volume, and HE staining scores. EA could significantly inhibit the expression of CD34, promoting apoptosis of synovial cells in the joint synovial tissue of AA rats. The expression of Notch1 signaling pathway proteins and mRNAs (Notch1, Hes1, TGF-β, and bFGF) were markedly downregulated by EA treatment.

Conclusions: These results prove that EA attenuates synovial angiogenesis by inhibiting the Notch1 signaling pathway in AA rat models. Based on our findings, we propose that EA is a promising complementary and alternative therapy in rheumatoid arthritis.

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