Liu Yu-Da, Peng Xiao, Chen Hao-Ran, Liu Xue-Song, Peng Li-Hua
College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, China.
Jinhua Institute, Zhejiang University, Jinhua, Zhejiang, China.
Front Pharmacol. 2024 Oct 22;15:1487183. doi: 10.3389/fphar.2024.1487183. eCollection 2024.
Rapid tissue reconstruction in acute and chronic injuries are challengeable, the inefficient repair mainly due to the difficulty in simultaneous promoting the regeneration of peripheral nerves and vascular, which are closely related. Main clinical medication strategy of tissue repair depends on different cytokines to achieve nerves, blood vessels or granulation tissue regeneration, respectively. However, their effect is still limited to single aspect with biorisk exists upon long-time use. Herein, for the first time, we have demonstrated that NA isolated from has potential to simultaneously promote both neurogenesis and angiogenesis and . First, NA was identified by NMR and FTIR structural characterization analysis. In a model of oxidative stress in neural cells induced by hydrogen peroxide, the cells viability of RSC96 and PC12 were protected from oxidative stress injury by NA. Similarly, based on the rat wound healing model, effective blood vessel formation and wound healing can be observed in tissue staining under NA treatment. In addition, according to the identification of nerve and vascular related markers in the wound tissue, the mechanism of NA promoting nerve regeneration lies in the upregulation of the secretion NGF, NF-200 and S100 protein, and NA treatment was also able to up-regulate VEGF and CD31 to directly promote angiogenesis during wound healing. This study provides an important candidate drug molecules for acute or chronic wound healing and nerve vascular synchronous regeneration.
急性和慢性损伤中的快速组织重建具有挑战性，修复效率低下主要是由于难以同时促进密切相关的外周神经和血管的再生。组织修复的主要临床用药策略依赖于不同的细胞因子来分别实现神经、血管或肉芽组织的再生。然而，它们的作用仍局限于单一方面，长期使用存在生物风险。在此，我们首次证明从[具体来源]分离出的NA有潜力同时促进神经发生和血管生成。首先，通过核磁共振（NMR）和傅里叶变换红外光谱（FTIR）结构表征分析鉴定了NA。在过氧化氢诱导的神经细胞氧化应激模型中，NA保护了RSC96和PC12细胞的活力免受氧化应激损伤。同样，基于大鼠伤口愈合模型，在NA处理后的组织染色中可观察到有效的血管形成和伤口愈合。此外，根据伤口组织中神经和血管相关标志物的鉴定，NA促进神经再生的机制在于上调神经生长因子（NGF）、神经丝蛋白200（NF - 200）和S100蛋白的分泌，并且NA处理还能够上调血管内皮生长因子（VEGF）和血小板内皮细胞黏附分子1（CD31）以在伤口愈合过程中直接促进血管生成。本研究为急性或慢性伤口愈合以及神经血管同步再生提供了一种重要的候选药物分子。
