电针刺激足三里（ST36）和悬钟（GB39）对佐剂性关节炎大鼠滑膜血管生成的影响。
Efficacy of electroacupuncture stimulating Zusanli (ST36) and Xuanzhong (GB39) on synovial angiogenesis in rats with adjuvant arthritis.
机构信息
School of Acupuncture-Moxibustion and Tuina, Chengdu University of Traditional Chinese Medicine, Chengdu 610075, China.
Vocational Training Department, Acupuncture and Moxibustion School Affiliated to Chengdu University of Traditional Chinese Medicine, Chengdu 610075, China.
出版信息
J Tradit Chin Med. 2023 Oct;43(5):955-962. doi: 10.19852/j.cnki.jtcm.20221111.002.
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.
目的
观察电针刺激足三里（ST36）和悬钟（GB39）穴对佐剂性关节炎（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，大鼠给予电针刺激足三里（ST36）和悬钟（GB39）穴位，隔日一次，共 16 天。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。观察血管生成标志物 CD34 表达和滑膜细胞凋亡。随后检测 Notch1、Hairy 和 Enhancer of Split 同源物 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
我们发现电针显著降低了关节炎指数评分、爪体积和 HE 染色评分。电针能显著抑制 AA 大鼠关节滑膜组织中 CD34 的表达，促进滑膜细胞凋亡。电针治疗显著下调 Notch1 信号通路蛋白及其 mRNA（Notch1、Hes1、TGF-β和 bFGF）的表达。
结论
这些结果证明电针通过抑制 AA 大鼠模型中的 Notch1 信号通路来减轻滑膜血管生成。基于我们的发现，我们提出电针是类风湿关节炎的一种有前途的补充和替代治疗方法。
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