Salvianolic acid B improves diabetic skin wound repair through Pink1/Parkin-mediated mitophagy.

IF 2.5 4区 医学 Q3 ENDOCRINOLOGY & METABOLISM
Chunling Zhang, Jie Xiang, Gengxin Wang, Tietao Di, Lu Chen, Wei Zhao, Lianggang Wei, Shiyong Zhou, Xueli Wu, Yun Zhang, Yanhui Wang, Haiyan Liu
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Abstract

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.

丹酚酸 B 通过 Pink1/Parkin 介导的有丝分裂改善糖尿病皮肤伤口修复
糖尿病皮肤伤口是一个令人不安且发展迅速的临床问题。在此,我们研究了丹酚酸 B(Sal B)对糖尿病伤口愈合过程的影响。服用丹酚酸 B 后,组织病理学损伤通过 H&E 和 Masson 染色法进行检测,CD34、细胞凋亡和有丝分裂标记物通过免疫荧光、免疫组织化学和 Western 印迹法进行检测。测量了高糖(HG)诱导的 HMEC-1 细胞的迁移、增殖和线粒体功能。研究了 si-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的炎症细胞浸润并促进了血管生成。Sal B可改善糖尿病皮肤伤口组织和HG诱导的HMEC-1细胞的凋亡和线粒体自噬。抑制Parkin可抑制HMEC-1细胞的迁移促进细胞凋亡和有丝分裂。这一发现证明了 Sal B 通过 Pink1/Parkin 介导的有丝分裂促进了糖尿病皮肤伤口的修复,增进了我们对糖尿病伤口愈合过程的了解。
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来源期刊
Archives of Physiology and Biochemistry
Archives of Physiology and Biochemistry ENDOCRINOLOGY & METABOLISM-PHYSIOLOGY
CiteScore
6.90
自引率
3.30%
发文量
21
期刊介绍: Archives of Physiology and Biochemistry: The Journal of Metabolic Diseases is an international peer-reviewed journal which has been relaunched to meet the increasing demand for integrated publication on molecular, biochemical and cellular aspects of metabolic diseases, as well as clinical and therapeutic strategies for their treatment. It publishes full-length original articles, rapid papers, reviews and mini-reviews on selected topics. It is the overall goal of the journal to disseminate novel approaches to an improved understanding of major metabolic disorders. The scope encompasses all topics related to the molecular and cellular pathophysiology of metabolic diseases like obesity, type 2 diabetes and the metabolic syndrome, and their associated complications. Clinical studies are considered as an integral part of the Journal and should be related to one of the following topics: -Dysregulation of hormone receptors and signal transduction -Contribution of gene variants and gene regulatory processes -Impairment of intermediary metabolism at the cellular level -Secretion and metabolism of peptides and other factors that mediate cellular crosstalk -Therapeutic strategies for managing metabolic diseases Special issues dedicated to topics in the field will be published regularly.
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