目的 探讨体外冲击波（ESWT）对高糖诱导的人主动脉内皮细胞（HAECs）发生内皮-间充质转化（EndMT）的影响及其可能机制。 方法 采用高糖培养基构建HAECs的EndMT模型，分为正常对照组（CON组）、对照+冲击波组（CE组）、高糖组（HG组）、冲击波+高糖组（ESWT组）、Snail抑制剂组（CYD19组），培养基葡萄糖浓度为5 mmol/L（CON组、CE组）、25 mmol/L（HG组、ESWT组、CYD19组）。培养7 d后，对干预组细胞重新悬浮后施以冲击波（8 Hz、0.1 mJ/mm2、1 000次脉冲，每2 d 1次，共3次）干预治疗。通过茜素红染色检测钙盐沉积；Western blot与免疫荧光检测血管内皮细胞标志物（CD31、VEGF）、间充质标志物（α?SMA、FSP?1、OPG）表达；Western blot检测锌指转录因子（Snail）的表达及MAPK通路（ERK1/2、p38）总蛋白与磷酸化水平。 结果 茜素红染色显示，与CON组相比，HG组钙盐沉积显著增加，ESWT组钙盐沉积明显减少。相较于CON组，HG组CD31、VEGF表达显著降低，α?SMA、FSP?1、OPG表达显著升高，ERK1/2、p38总蛋白及磷酸化水平、Snail表达均显著上调；与HG组相比，ESWT组CD31、VEGF表达显著上调，α?SMA、FSP?1、OPG表达下调，同时ERK1/2、p38的表达与磷酸化受抑制，Snail蛋白水平降低。此外，与HG组相比，ESWT组及CYD19组Snail蛋白表达水平均显著降低。 结论 ESWT介导的生物学效应可改善高糖环境下HAECs的钙化进程，其作用机制可能是ESWT通过下调MAPK信号通路中p38、ERK1/2的表达及磷酸化水平，抑制下游转录因子Snail的表达，进而逆转EndMT。

Objective To investigate the effect of extracorporeal shock wave therapy （ESWT） on high glucose-induced endothelial?mesenchymal transition （EndMT） in human aortic endothelial cells （HAECs） and explore its potential mechanism. Methods HAECs were cultured in a high?glucose medium to establish an EndMT model. The cells were divided into five distinct groups： the normal control group （CON）， the control+shockwave group （CE）， the high?glucose group （HG）， the high?glucose + ESWT group （ESWT）， and the Snail inhibitor group （CYD19）. In the CON and CE groups， the glucose concentration was set at 5 mmol/L， while in the HG， ESWT， and CYD19 groups， it was 25 mmol/L. After culturing the cells for 7 days， the cells in the intervention groups were resuspended and subjected to shockwave treatment （8 Hz， 0.1 mJ/mm2， 1 000 pulses） once every 2 days， with a total of 3 treatments. Calcium deposition was detected using Alizarin Red S staining. The expression levels of endothelial markers （CD31， VEGF） and mesenchymal markers （α?SMA， FSP?1， OPG） were determined through Western blot and immunofluorescence analyses. Additionally， the expression of Snail， along with the total and phosphorylated levels of ERK1/2 and p38， were also measured. Results Alizarin Red S staining demonstrated that calcium deposition was significantly elevated in the HG group when compared with the CON group， and ESWT intervention notably reduced calcium deposition. In comparison with the CON group， the HG group showed a significant decrease in the expression of CD31 and VEGF， but an increase in the expression of α?SMA， FSP?1， and OPG. Meanwhile， the total and phosphorylated levels of ERK1/2 and p38， along with Snail expression， were significantly upregulated. When compared with the HG group， ESWT intervention significantly upregulated the expression of CD31 and VEGF， downregulated the expression of α?SMA， FSP?1， and OPG， inhibited the expression and phosphorylation of ERK1/2 and p38， and reduced the levels of Snail protein. Moreover， Snail expression was significantly decreased in both the ESWT and CYD19 groups as compared with the HG group. Conclusions The biological effects mediated by ESWT can effectively ameliorate the calcification of HAECs in a high?glucose environment. The underlying mechanism is likely that ESWT downregulates the expression and phosphorylation of p38 and ERK1/2 in the MAPK signaling pathway， thus inhibiting the expression of the downstream transcription factor Snail and reversing EndMT.