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目的:评价紫杉醇对肺动脉高压大鼠肥大细胞-趋化因子配体2(CCL2)-巨噬细胞轴的影响。方法:SPF级健康雄性SD大鼠30只，8～10周龄，体重180～220 g，采用随机数字表法分为3组(n n＝10)：对照组(C组)、肺动脉高压组(PH组)和紫杉醇组(PTX组)。采用皮下注射野百合碱60 mg/kg的方法制备大鼠肺动脉高压模型，模型制备开始后25 d，PTX组经尾静脉注射紫杉醇2 mg/kg，1次/4 d，共4次。余2组注射等量生理盐水。模型制备后40 d，行平均肺动脉压(mPAP)测定。随后取心脏烘干后分别称重右心室(RV)和左心室加室间隔(LV+S)，计算Fulton指数。取左下肺叶，HE染色测算肺血管中膜厚度比值，免疫组化法计数每个血管周围Tryptasen +、CD68n +和CD163n +总细胞数，并计算平均值，计数并计算血管Ki67阳性细胞数量百分比，测算肌化血管比例。ELISA法检测CCL2含量，Western blot法检测裂解caspase-3和Cyclin D1表达。n 结果:与C组比较，PH组和PTX组mPAP、Fulton指数、血管中膜厚度比值和肌化血管比例升高，Tryptasen +、CD68n +和CD163n +细胞数量增加，Ki67n +细胞百分比升高，肺组织裂解caspase-3表达下调，PH组肺组织Cyclin D1表达上调(n P0.05)；与PH组比较，PTX组mPAP、Fulton指数、血管中膜厚度比值及肌化血管比例降低，Tryptasen +、CD68n +和CD163n +细胞数量减少，Ki67n +细胞百分比降低，肺组织CCL2和Cyclin D1表达下调，裂解caspase-3表达上调(n P<0.05)。n 结论:紫杉醇缓解大鼠肺动脉高压的机制与抑制肥大细胞-CCL2-巨噬细胞轴有关。“,”Objective:To evaluate the effect of paclitaxel on the mast cell-CCL2-macrophage axis in rats with pulmonary hypertension.Methods:Thirty SPF-grade healthy male Sprague-Dawley rats, aged 8-10 weeks, weighing 180-220 g, were divided into 3 groups (n n=10 each) using a random number table method: control group (group C), pulmonary hypertension group (group PH), and paclitaxel group (group PTX). The model of pulmonary hypertension was established by subcutaneous injection of monocrotaline 60 mg/kg in rats.At 25 days after establishing the models, paclitaxel 2 mg/kg was injected via the tail vein once every four days, for 4 times in total in group PTX.The equal volume of normal saline was injected in the remaining 2 groups.The mean pulmonary artery pressure (mPAP) was performed at 40 days after establishing the model.The heart was removed and dried, the right ventricle (RV) and left ventricle plus ventricular septum (LV+ S) was weighed, and the Fulton index [RV/(LV+ S)] was calculated.The inferior lobe of left lung was taken, the ratio of media wall thickness of pulmonary vessels was calculated by HE staining, the number of Tryptasen + , CD68n + , CD163n + , and Ki67n + cells was recorded by immunohistochemistry, the mean value was calculated, the percentage of Ki67-positive cells in blood vessels was recorded, and the proportion of muscularized blood vessels was calculated.The content of CCL2 was measured by enzyme-linked immunosorbent assay, and the expression of cleaved caspase-3 and Cyclin D1 was detected by Western blot.n Results:Compared with group C, the mPAP, Fulton index, ratio of media wall thickness, proportion of muscularized blood vessels, the number of Tryptasen + , CD68n + and CD163n + cells and percentage of Ki67n + cells were significantly increased, and the expression of cleaved caspase-3 was down-regulated in PH and PTX groups (n P<0.05), the expression of Cyclin D1 was significantly up-regulated in group PH (n P0.05). Compared with group PH, the mPAP, Fulton index, ratio of media wall thickness, percentage of muscularized blood vessels, the number of Tryptasen + , CD68n + and CD163n + cells and percentage of Ki67n + cells were significantly decreased, the expression of CCL2 and Cyclin D1 was down-regulated, and the expression of cleaved caspase-3 was up-regulated in group PTX (n P<0.05).n Conclusion:The mechanism by which paclitaxel alleviates pulmonary hypertension is related to inhibiting the mast cell-CCL2-macrophage axis in rats.