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阿卡波糖通过Akt/eNOS信号通路促进小鼠伤口愈合。

Acarbose Accelerates Wound Healing via Akt/eNOS Signaling in Mice.

作者信息

Han Xue, Deng Yaping, Yu Jiawen, Sun Yuannan, Ren Guofei, Cai Jian, Zhu Jianjun, Jiang Guojun

机构信息

Department of Pharmacy, Xiaoshan Hospital, Hangzhou, Zhejiang 311202, China.

出版信息

Oxid Med Cell Longev. 2017;2017:7809581. doi: 10.1155/2017/7809581. Epub 2017 Mar 8.

DOI:10.1155/2017/7809581
PMID:28373902
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5360971/
Abstract

Refractory wound is a dreaded complication of diabetes and is highly correlated with EPC dysfunction caused by hyperglycemia. Acarbose is a widely used oral glucose-lowering drug exclusively for T2DM. Previous studies have suggested the beneficial effect of acarbose on improving endothelial dysfunction in patients with T2DM. However, no data have been reported on the beneficial efficacy of acarbose in wound healing impairment caused by diabetes. We herein investigated whether acarbose could improve wound healing in T2DM mice and the possible mechanisms involved. Acarbose hastened wound healing and enhanced angiogenesis, accompanied by increased circulating EPC number in mice. In vitro, a reversed BM-EPC dysfunction was observed after the administration of acarbose in mice, as reflected by tube formation assay. In addition, a significantly increased NO production was also witnessed in BM-EPCs from acarbose treated mice, with decreased O levels. Akt inhibitor could abolish the beneficial effect of acarbose on high glucose induced EPC dysfunction in vitro, accompanied by reduced eNOS activation. Acarbose displayed potential effect in promoting wound healing and improving angiogenesis in T2DM mice, which was possibly related to the Akt/eNOS signaling pathway.

摘要

难治性伤口是糖尿病可怕的并发症,与高血糖引起的内皮祖细胞(EPC)功能障碍高度相关。阿卡波糖是一种广泛用于2型糖尿病(T2DM)的口服降糖药物。先前的研究表明阿卡波糖对改善T2DM患者的内皮功能障碍具有有益作用。然而,尚无关于阿卡波糖对糖尿病所致伤口愈合受损有益疗效的数据报道。我们在此研究了阿卡波糖是否能改善T2DM小鼠的伤口愈合以及可能涉及的机制。阿卡波糖加速了伤口愈合并增强了血管生成,同时小鼠循环EPC数量增加。在体外,给予阿卡波糖后观察到小鼠骨髓来源的EPC(BM-EPC)功能障碍得到逆转,这通过管腔形成试验得以体现。此外,在接受阿卡波糖治疗的小鼠的BM-EPC中还观察到一氧化氮(NO)产生显著增加,氧水平降低。Akt抑制剂可消除阿卡波糖对体外高糖诱导的EPC功能障碍的有益作用,同时内皮型一氧化氮合酶(eNOS)激活减少。阿卡波糖在促进T2DM小鼠伤口愈合和改善血管生成方面显示出潜在作用,这可能与Akt/eNOS信号通路有关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bec4/5360971/c64d1ecccb13/OMCL2017-7809581.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bec4/5360971/041cf6166a50/OMCL2017-7809581.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bec4/5360971/18bcac1f306e/OMCL2017-7809581.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bec4/5360971/4b3f782be970/OMCL2017-7809581.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bec4/5360971/84f61e174a3e/OMCL2017-7809581.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bec4/5360971/9c37654a8edc/OMCL2017-7809581.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bec4/5360971/aa848c048466/OMCL2017-7809581.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bec4/5360971/c64d1ecccb13/OMCL2017-7809581.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bec4/5360971/041cf6166a50/OMCL2017-7809581.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bec4/5360971/18bcac1f306e/OMCL2017-7809581.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bec4/5360971/4b3f782be970/OMCL2017-7809581.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bec4/5360971/84f61e174a3e/OMCL2017-7809581.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bec4/5360971/9c37654a8edc/OMCL2017-7809581.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bec4/5360971/aa848c048466/OMCL2017-7809581.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bec4/5360971/c64d1ecccb13/OMCL2017-7809581.007.jpg

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