Electroacupuncture on ST36 and GB39 Acupoints Inhibits Synovial Angiogenesis via Downregulating HIF-1 alpha/VEGF Expression in a Rat Model of Adjuvant Arthritis
Electroacupuncture on ST36 and GB39 Acupoints Inhibits Synovial Angiogenesis via Downregulating HIF-1 alpha/VEGF Expression in a Rat Model of Adjuvant Arthritis
复制标题
电针 ST36 和 GB39 穴位通过下调佐剂性关节炎大鼠模型中 HIF-1 α/VEGF 表达抑制滑膜血管生成
DOI：
10.1155/2019/5741931
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发表时间：
2019
影响因子：
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通讯作者：
Jiang Jianzhen
中科院分区：
文献类型：
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作者：
Zhu Jun;Su Chengguo;Chen Yuzhou;Hao Xinyu;Jiang Jianzhen
缺氧诱导因子-1 α（HIF-1α）和血管内皮生长因子（VEGF）在类风湿关节炎（RA）滑膜血管生成中起关键作用。方法SD道利大鼠随机分为4组：对照组、佐剂性关节炎（AA）组、AA+电针组和AA+假电针组。双侧后足垫注射弗氏完全佐剂诱导AA模型。注射后3d，电针组电针足三里、悬钟穴，隔日1次，共8次，假电针组给予假电针治疗。测量每只动物的关节炎评分、爪体积和H&E染色。免疫组化法观察踝关节滑膜组织中CD 34的表达。结果与AA组比较，电针组大鼠关节炎评分、足爪体积、滑膜组织病理损伤均明显减轻，关节炎模型组大鼠关节炎评分、足爪体积、滑膜组织病理损伤均明显减轻。电针还能显著抑制AA大鼠滑膜血管生成，表现为CD 34阳性表达减少。电针还能显著降低AA大鼠滑膜组织中HIF-1α和VEGF的mRNA和蛋白水平。滑膜组织中CD 34的表达与HIF-1α和VEGF蛋白水平呈正相关。电针足三里、足三里穴可通过下调HIF-1α/VEGF表达，有效抑制AA大鼠滑膜血管生成。
IntroductionThe hypoxia inducible factor‐1α(HIF‐1α) and vascular endothelial growth factor (VEGF) play a key role in synovial angiogenesis in rheumatoid arthritis (RA). Therefore, this study aimed to test the hypothesis that electroacupuncture (EA) may inhibit RA synovial angiogenesis via HIF‐1α/VEGF expression.MethodsSprague‐Dawley rats were randomly distributed to 4 groups: control, adjuvant arthritis (AA), AA+electroacupuncture (AA+EA), and AA+sham EA groups. AA model was induced by injection of Freund′s complete adjuvant in bilateral hind footpad. 3 days after injection, EA was delivered to the acupoints Zusanli (ST 36) and Xuanzhong (GB 39) once every two days for a total of 8 times in the AA+EA group, while sham EA treatment was applied in the AA+sham EA group. The arthritis score, paw volume, and H&E staining for each animal were measured. CD34 expression in synovial tissue of ankle joint was observed by immunohistochemistry. HIF‐1αand VEGF mRNA and protein levels in synovial tissue were determined by real‐time quantitative PCR and Western blot, respectively.ResultsCompared with rats in AA group, EA stimulation significantly decreased arthritis scores, paw volume, and pathological damage of synovial tissues. Moreover, EA markedly suppressed the synovial angiogenesis of AA rats, as evidenced by reduced CD34 positive expression. Furthermore, EA significantly reduced HIF‐1αand VEGF mRNA and protein levels in synovial of AA rats. Finally, the CD34 expression in synovial tissue was positively correlated with HIF‐1αand VEGF protein levels.Conclusion. EA on ST36 and GB39 acupoints can effectively inhibit synovial angiogenesis in the AA rat model via downregulating HIF‐1α/VEGF expression.