Analysis and Testing Center, School of Pharmacy, Southwest Medical University, Luzhou, Sichuan 646000, China.
Department of Nuclear Medicine, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan 646000, China.
Colloids Surf B Biointerfaces. 2024 Nov;243:114159. doi: 10.1016/j.colsurfb.2024.114159. Epub 2024 Aug 10.
After myocardial ischemia/reperfusion injury (MI/RI), endothelial cell injury causes impaired angiogenesis and obstruction of microcirculation, resulting in an inflammatory outburst that exacerbates the damage. Therefore, synergistic blood vessel repair and inflammation inhibition are effective therapeutic strategies. In this study, we developed a platelet membrane (PM)-encapsulated baicalin nanocrystalline (BA NC) nanoplatform with a high drug load, BA NC@PM, which co-target to endothelial cells and macrophages through the transmembrane proteins of the PM to promote angiogenesis and achieve anti-inflammatory effects. In vitro cell scratch assays and transwell assay manifested that BA NC@PM could promote endothelial cell migration, as well as increase mRNA expression of CD31 and VEGF in the heart after treatment of MI/RI mice, suggesting its favorable vascular repair function. In addition, the preparation significantly reduced the expression of pro-inflammatory factors and increased the expression of anti-inflammatory factors in plasma, promoting the polarization of macrophages. Our study highlights a strategy for enhancing the treatment of MI/RI by promoting angiogenesis and regulating macrophage polarization via the biomimetic BA NC@PM nanoplatform.
心肌缺血/再灌注损伤（MI/RI）后，内皮细胞损伤导致血管生成受损和微循环阻塞，引发炎症爆发，从而加重损伤。因此，协同的血管修复和炎症抑制是有效的治疗策略。在本研究中，我们开发了一种载药量高的血小板膜（PM）包裹黄芩素纳米结晶（BA NC）纳米平台，即 BA NC@PM，通过 PM 的跨膜蛋白共同靶向内皮细胞和巨噬细胞，促进血管生成并发挥抗炎作用。体外细胞划痕实验和 Transwell 实验表明，BA NC@PM 可促进内皮细胞迁移，并增加 MI/RI 小鼠心脏中 CD31 和 VEGF 的 mRNA 表达，提示其具有良好的血管修复功能。此外，该制剂还显著降低了促炎因子的表达，增加了抗炎因子在血浆中的表达，促进了巨噬细胞的极化。我们的研究强调了通过仿生 BA NC@PM 纳米平台促进血管生成和调节巨噬细胞极化来增强 MI/RI 治疗的策略。
