Table 1_Tanshinone IIA accelerates zebrafish venous vascular repair via macrophage recruitment through the CXCR4A–CXCL12B signaling axis.docx

BackgroundVascular injury is a major contributor to the development of cardiovascular diseases. Following vascular damage, macrophages migrate to the injury site and, during the later stages of vascular repair, secrete cytokines such as interleukin-10 (IL-10) and transforming growth factor-β1a (TGFB1A), thereby promoting vascular regeneration. Previous studies have demonstrated that macrophage recruitment to sites of tissue injury is mediated by the CXCR4A-CXCL12B signaling axis. In a screening of traditional Chinese medicinal herbs for cardiovascular therapeutic potential, Salvia miltiorrhiza root was identified as a promising source of bioactive compounds capable of enhancing vascular repair through modulation of the CXCR4A-CXCL12B axis.
MethodsEstablishing a vascular injury model in transgenic zebrafish lines Tg (flk1:eGFP; gata1:dsRed) using a two-photon microscopy laser system. Dynamic monitoring of vascular repair via two-photon microscopy. Evaluate macrophage migration capacity in a Tg (mpeg1:eGFP) zebrafish vascular injury model using confocal microscopy. Detection of il-10 and tgfb1a expression released by macrophages via qPCR experiments. Detect CXCR4A-CXCL12B expression at the site of zebrafish vascular injury via fluorescence in situ hybridization coupled with antibody staining.
ResultsWe confirm that compounds from the selected extract promote macrophage migration to vascular injury sites by upregulating the CXCR4A-CXCR12B signaling axis. This process accelerates repair of damaged blood vessels in zebrafish by inducing the release of cytokines such as il-10 and tgfb1a.
ConclusionsThis study confirms that Salvia miltiorrhiza, a traditional Chinese medicinal plant, is a valuable source of bioactive compounds with pro-angiogenic properties. Our findings provide scientific support for the traditional use of Salvia miltiorrhiza active components in treating vascular injuries.

背景：血管损伤是心血管疾病发生的主要诱因。血管损伤发生后，巨噬细胞会迁移至损伤部位，并在血管修复的后期阶段分泌白细胞介素-10（interleukin-10，IL-10）、转化生长因子-β1a（transforming growth factor-β1a，TGFB1A）等细胞因子，进而促进血管再生。既往研究表明，组织损伤部位的巨噬细胞募集过程由CXCR4A-CXCL12B信号轴介导。在针对具有心血管治疗潜力的中草药开展筛选时，研究人员发现丹参（Salvia miltiorrhiza）根中含有可通过调控CXCR4A-CXCL12B轴增强血管修复的活性成分，具备良好的应用前景。
方法：采用双光子显微镜激光系统，在转基因斑马鱼品系Tg(flk1:eGFP; gata1:dsRed)中构建血管损伤模型。通过双光子显微镜动态监测血管修复进程。利用共聚焦显微镜，在Tg(mpeg1:eGFP)斑马鱼血管损伤模型中评估巨噬细胞的迁移能力。通过定量聚合酶链反应（quantitative PCR，qPCR）实验检测巨噬细胞分泌的il-10与tgfb1a的表达水平。采用荧光原位杂交联合抗体染色技术，检测斑马鱼血管损伤部位CXCR4A-CXCL12B的表达情况。
结果：本研究证实，所筛选提取物中的活性成分可通过上调CXCR4A-CXCR12B信号轴，促进巨噬细胞向血管损伤部位迁移；该过程可诱导il-10、tgfb1a等细胞因子的释放，进而加速斑马鱼受损血管的修复。
结论：本研究证实，中草药丹参（Salvia miltiorrhiza）是一种具备促血管生成活性的珍贵活性化合物来源。本研究结果为丹参活性成分用于治疗血管损伤的传统应用提供了科学依据。