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硫化氢可改善糖尿病小鼠缺血内收肌的血管生成及伤口愈合。

Hydrogen sulfide improves vessel formation of the ischemic adductor muscle and wound healing in diabetic mice.

作者信息

Wang Guo-Guang, Li Wei

机构信息

Department of Pathophysiology, Wannan Medical College, Wuhu, China.

出版信息

Iran J Basic Med Sci. 2019 Oct;22(10):1192-1197. doi: 10.22038/ijbms.2019.36551.8709.

DOI:10.22038/ijbms.2019.36551.8709
PMID:31998462
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6885384/
Abstract

OBJECTIVES

It has been demonstrated that hydrogen sulfide plays a vital role in physiological and pathological processes such as regulating inflammation, oxidative stress, and vessel relaxation. The aim of the study was to explore the effect of hydrogen sulfide on angiogenesis in the ischemic adductor muscles of type 2 diabetic mice and ischemic diabetic wound healing.

MATERIALS AND METHODS

The femoral arteries of diabetic mice were isolated and ligated for preparation of ischemic hind limb model. Round incision was made on ischemic and non-ischemic limbs. The wounds were treated with sodium bisulfide (hydrogen sulfide donor). Real-time PCR and Western blotting were used to measure transcription of vascular endothelial growth factor (VEGF), epidermal growth factor (EGF), platelet derived growth factor (PDGF), hypoxia inducible factor-1α (HIF-1α) and endothelial nitric oxide synthase (eNOS) and protein expression of VEGF, VEGF receptor (VEGFR) and PDGF, PDGF receptor (PDGFR), respectively. Angiogenesis and morphological changes in adductor muscles were observed.

RESULTS

Hydrogen sulfide significantly increased transcription of VEGF, EGF, PDGF, HIF-1α, eNOS and protein expression of VEGF, PDGF, and phosphorylated VEGFR and PDGFR. Treatment with hydrogen sulfide significantly improved ischemic wound healing and formation of granulation tissue, and increased the number of small vessels in the ischemic adductor muscles.

CONCLUSION

Our data suggested that hydrogen sulfide attenuated injury of ischemic adductor muscle, and promoted the ischemic diabetic wound healing via modulating angiogenesis in type 2 diabetic mice.

摘要

目的

已证实硫化氢在调节炎症、氧化应激和血管舒张等生理和病理过程中发挥着至关重要的作用。本研究的目的是探讨硫化氢对2型糖尿病小鼠缺血内收肌血管生成及缺血性糖尿病伤口愈合的影响。

材料与方法

分离并结扎糖尿病小鼠的股动脉以制备缺血后肢模型。在缺血和非缺血肢体上做圆形切口。伤口用硫氢化钠(硫化氢供体)处理。采用实时定量聚合酶链反应(Real-time PCR)和蛋白质免疫印迹法(Western blotting)分别检测血管内皮生长因子(VEGF)、表皮生长因子(EGF)、血小板衍生生长因子(PDGF)、缺氧诱导因子-1α(HIF-1α)和内皮型一氧化氮合酶(eNOS)的转录水平,以及VEGF、VEGF受体(VEGFR)、PDGF、PDGF受体(PDGFR)的蛋白表达水平。观察内收肌的血管生成和形态变化。

结果

硫化氢显著增加VEGF、EGF、PDGF、HIF-1α、eNOS的转录水平,以及VEGF、PDGF、磷酸化VEGFR和PDGFR的蛋白表达。硫化氢处理显著改善缺血伤口愈合和肉芽组织形成,并增加缺血内收肌中小血管的数量。

结论

我们的数据表明,硫化氢减轻了缺血内收肌的损伤,并通过调节2型糖尿病小鼠的血管生成促进了缺血性糖尿病伤口的愈合。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d8a/6885384/44684956da82/IJBMS-22-1192-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d8a/6885384/7e4d0127d007/IJBMS-22-1192-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d8a/6885384/1c81161e71d5/IJBMS-22-1192-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d8a/6885384/6c203f6b0e21/IJBMS-22-1192-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d8a/6885384/093671f854ce/IJBMS-22-1192-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d8a/6885384/44684956da82/IJBMS-22-1192-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d8a/6885384/7e4d0127d007/IJBMS-22-1192-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d8a/6885384/1c81161e71d5/IJBMS-22-1192-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d8a/6885384/6c203f6b0e21/IJBMS-22-1192-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d8a/6885384/093671f854ce/IJBMS-22-1192-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d8a/6885384/44684956da82/IJBMS-22-1192-g005.jpg

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