Zhang Chunling, Xiang Jie, Wang Gengxin, Di Tietao, Chen Lu, Zhao Wei, Wei Lianggang, Zhou Shiyong, Wu Xueli, Zhang Yun, Wang Yanhui, Liu Haiyan
Department of Nutrition, The Second Affiliated Hospital of Guizhou University of Traditional Chinese Medicine, Guiyang, China.
Department of Monitoring, Guizhou Center for Disease Control and Prevention, Institute of Chronic Disease Prevention and Treatment, Guiyang, China.
Arch Physiol Biochem. 2025 Feb;131(1):40-51. doi: 10.1080/13813455.2024.2387693. Epub 2024 Aug 5.
Diabetic skin wound is a disturbing and rapidly evolving clinical issue. Here, we investigated how salvianolic acid B (Sal B) affected the diabetic wound healing process. Following Sal B administration, histopathological damage was investigated by H&E and Masson staining, and CD34, apoptosis and mitophagy markers were measured by immunofluorescence, immunohistochemistry, and western blotting. Migration, proliferation, and mitochondrial function of high glucose (HG) -induced HMEC-1 cells were measured. The effects of si-Parkin on endothelial cell migration, apoptosis and mitochondrial autophagy were examined. Sal B alleviated inflammatory cell infiltration and promoted angiogenesis in skin wound tissue. Apoptosis and mitophagy were ameliorated by Sal B in diabetic skin wound tissues and HG-induced HMEC-1 cells. Parkin inhibition impaired the migratorypromoted cell apoptosis and inhibited mitophagy of HMEC-1 cells. This finding demonstrated that Sal B promoted diabetic skin wound repair via Pink1/Parkin-mediated mitophagy, improved our understanding of the diabetic wound healing process.
糖尿病皮肤伤口是一个令人困扰且迅速演变的临床问题。在此，我们研究了丹酚酸B（Sal B）如何影响糖尿病伤口愈合过程。给予Sal B后，通过苏木精-伊红（H&E）和Masson染色研究组织病理学损伤，并通过免疫荧光、免疫组织化学和蛋白质印迹法检测CD34、凋亡和线粒体自噬标志物。检测高糖（HG）诱导的人微血管内皮细胞-1（HMEC-1）细胞的迁移、增殖和线粒体功能。研究小干扰RNA（si）-帕金蛋白（Parkin）对内皮细胞迁移、凋亡和线粒体自噬的影响。Sal B减轻了皮肤伤口组织中的炎性细胞浸润并促进了血管生成。Sal B改善了糖尿病皮肤伤口组织和HG诱导的HMEC-1细胞中的凋亡和线粒体自噬。抑制Parkin会损害迁移促进细胞凋亡并抑制HMEC-1细胞的线粒体自噬。这一发现表明，Sal B通过Pink1/Parkin介导的线粒体自噬促进糖尿病皮肤伤口修复，增进了我们对糖尿病伤口愈合过程的理解。
