IMR Press / FBL / Volume 21 / Issue 5 / DOI: 10.2741/4439

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.

Open Access Article

Diazoxide accelerates wound healing by improving EPC function

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1 Department of Pharmacology, School of Pharmacy, Second Military Medical University, Shanghai 200433, China
2 Department of Pharmacy, Shanghai Tenth People’s Hospital, Tongji University, Shanghai 200072, China
3 Department of Pharmacy, Zhejiang Xiaoshan Hospital, Zhejiang 311202, China
Front. Biosci. (Landmark Ed) 2016, 21(5), 1039–1051; https://doi.org/10.2741/4439
Published: 1 June 2016
Abstract

Endothelial cell dysfunction is the primary cause of microvascular complications in diabetes. Diazoxide enables beta cells to rest by reversibly suppressing glucose-induced insulin secretion by opening ATP-sensitive K+ channels in the beta cells. This study investigated the role of diazoxide in wound healing in mice with streptozotocin (STZ)-induced diabetes and explored the possible mechanisms of its effect. Compared to the controls, mice with STZ-induced diabetes exhibited significantly impaired wound healing. Diazoxide treatment (30 mg/kg/d, intragastrically) for 28 days accelerated wound closure and stimulated angiogenesis in the diabetic mice. Circulating endothelial progenitor cells (EPCs) increased significantly in the diazoxide-treated diabetic mice. The adhesion, migration, and tube formation abilities of bone marrow (BM)-EPCs were impaired by diabetes, and these impairments were improved by diazoxide treatment. The expression of both p53 and TSP-1 increased in diabetic mice compared to that in the controls, and these increases were inhibited significantly by diazoxide treatment. In vitro, diazoxide treatment improved the impaired BM-EPC function and diminished the increased expression of p53 and TSP-1 in cultured BM-EPCs caused by high glucose levels. We conclude that diazoxide improved BM-EPC function in mice with STZ-induced diabetes, possibly via a p53-and TSP-1-dependent pathway.

Keywords
Diabetes
Diazoxide
Wound Healing
Endothelial Progenitor Cells
p53
TSP-1
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