PDF(Pubmed)
Abstract：
Previous reports have established that rESWT fosters angiogenesis, yet the mechanism by which rESWT promotes cerebral angiogenesis remains elusive. rESWT stimulated HUVECs proliferation as evidenced by the CCK-8 test, with an optimal dosage of 2.0 Bar, 200 impulses, and 2 Hz. The tube formation assay of HUVECs revealed that tube formation peaked at 36 h post-rESWT treatment, concurrent with the lowest expression level of Bach1, as detected by both Western blot and immunofluorescence. The expression level of Wnt3a, β-catenin, and VEGF also peaked at 36 h. A Bach1 overexpression plasmid was transfected into HUVECs, resulting in a decreased expression level of Wnt3a, β-catenin, and VEGF. Upon treatment with rESWT, the down-regulation of Wnt3a, β-catenin, and VEGF expression in the transfected cells was reversed. The Wnt/β-catenin inhibitor DKK-1 was utilized to suppress Wnt3a and β-catenin expression, which led to a concurrent decrease in VEGF expression. However, rESWT treatment could restore the expression of these three proteins, even in the presence of DKK-1. Moreover, in the established OGD model, it was observed that rESWT could inhibit the overexpression of Bach1 and enhance VEGF and VEGFR-2 expression under the OGD environment.
摘要：
以前的报道已经确定rESWT促进血管生成，然而，rESWT促进脑血管生成的机制仍然难以捉摸。CCK-8试验证明，rESWT刺激HUVECs增殖，最佳剂量为2.0巴，200个脉冲,和2Hz。HUVEC的管形成测定显示，管形成在rESWT处理后36小时达到峰值，同时通过蛋白质印迹和免疫荧光检测到Bach1的最低表达水平。Wnt3a的表达水平，β-连环蛋白，VEGF也在36小时达到峰值。将Bach1过表达质粒转染到HUVEC中，导致Wnt3a的表达水平降低，β-连环蛋白，和VEGF。用rESWT治疗后，WNT3a的下调，β-连环蛋白，转染细胞中VEGF的表达被逆转。Wnt/β-连环蛋白抑制剂DKK-1用于抑制Wnt3a和β-连环蛋白的表达，这导致VEGF表达的同时降低。然而,rESWT处理可以恢复这三种蛋白的表达，即使有DKK-1.此外，在建立的OGD模型中，观察到rESWT在OGD环境下可以抑制Bach1的过表达并增强VEGF和VEGFR-2的表达。
