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学科主题基础医学
Genistein accelerates refractory wound healing by suppressing superoxide and FoxO1/iNOS pathway in type 1 diabetes
Tie, Lu1,2; An, Yu1,2; Han, Jing1,2; Xiao, Yuan1,2; Xiaokaiti, Yilixiati1,2; Fan, Shengjun1,2; Liu, Shaoqiang1,2,3; Chen, Alex F.4,5; Li, Xuejun1,2
关键词Genistein Oxidative stress Diabetes iNOS FoxO1 Nitrotyrosine
刊名JOURNAL OF NUTRITIONAL BIOCHEMISTRY
2013
DOI10.1016/j.jnutbio.2012.02.011
24期:1页:88-96
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Biochemistry & Molecular Biology ; Nutrition & Dietetics
研究领域[WOS]Biochemistry & Molecular Biology ; Nutrition & Dietetics
关键词[WOS]NITRIC-OXIDE SYNTHASE ; SOY ISOFLAVONE GENISTEIN ; PROSTATE-CANCER CELLS ; OXIDATIVE STRESS ; ENDOTHELIAL-CELLS ; INDUCED DELAY ; MICE ; DYSFUNCTION ; DISEASE ; BETA
英文摘要

Refractory wounds in diabetic patients constitute a serious complication that often leads to amputation with limited treatment regimens. The present study was designed to determine the protective effect of the soy isoflavone genistein on diabetic wound healing and investigate underlying mechanisms. Streptozotocin (STZ)-induced type 1 diabetic mice with full-thickness excisional wounds received 0.2, 1 or 5 mg/kg/day of genistein via subcutaneous injection. Genistein dose-dependently rescued the delay of wound closure in diabetic mice. A dose of 5 mg/kg/day of genistein treatment significantly increased the mean perfusion rate, and in vitro treatment with genistein protected against high glucose-induced impairment of capillary tube formation in cultured endothelial cells. Diabetic conditions significantly increased superoxide anion (O-2(center dot-)) production and nitrotyrosine formation, and decreased nitrite levels in wound tissues. Genistein treatment at all doses normalized the elevated O-2(center dot-) production and nitrotyrosine formation, and reversed the attenuated nitrite level. In diabetic wound tissues, the inducible nitric oxide synthase (iNOS) was activated, and genistein administration prevented increased iNOS activity. Moreover, genistein attenuated diabetic cutaneous silent information regulator 1 and forkhead box 0 transcription factor 1 (FoxO1) levels and potentiated ac-FoxO1 in a dose-dependent manner. Genistein rescued the delayed wound healing and improved wound angiogenesis in STZ-induced type 1 diabetes in mice, at least in part, by suppression of FoxO1, iNOS activity and oxidative stress. (C) 2013 Elsevier Inc. All rights reserved.

语种英语
WOS记录号WOS:000312479700012
项目编号30901803 ; 91129727 ; 81020108031 ; 30973558 ; 30572202 ; 30901815 ; 20090001120046 ; 2009ZX09103-144 ; B07001
资助机构National Natural Science Foundation of China ; Research Fund for the Doctoral Program of Higher Education of China ; Major Specialized Research Fund from the Ministry of Science and Technology in China ; Research Fund from the Ministry of Education of China
引用统计
被引频次:20[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/67889
专题北京大学基础医学院_药理学系
北京大学医学部管理机构_医学部
北京大学基础医学院
作者单位1.Peking Univ, Inst Syst Biomed, Beijing 100191, Peoples R China
2.Peking Univ, Hosp 3, Beijing 100191, Peoples R China
3.Peking Univ, State Key Lab Nat & Biomimet Drugs, Dept Pharmacol, Sch Basic Med Sci, Beijing 100191, Peoples R China
4.Univ Pittsburgh, Sch Med, Dept Surg, Vasc Med Inst, Pittsburgh, PA 15213 USA
5.Univ Pittsburgh, Sch Med, McGowan Inst Regenerat Med, Pittsburgh, PA 15213 USA
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GB/T 7714
Tie, Lu,An, Yu,Han, Jing,et al. Genistein accelerates refractory wound healing by suppressing superoxide and FoxO1/iNOS pathway in type 1 diabetes[J]. JOURNAL OF NUTRITIONAL BIOCHEMISTRY,2013,24(1):88-96.
APA Tie, Lu.,An, Yu.,Han, Jing.,Xiao, Yuan.,Xiaokaiti, Yilixiati.,...&Li, Xuejun.(2013).Genistein accelerates refractory wound healing by suppressing superoxide and FoxO1/iNOS pathway in type 1 diabetes.JOURNAL OF NUTRITIONAL BIOCHEMISTRY,24(1),88-96.
MLA Tie, Lu,et al."Genistein accelerates refractory wound healing by suppressing superoxide and FoxO1/iNOS pathway in type 1 diabetes".JOURNAL OF NUTRITIONAL BIOCHEMISTRY 24.1(2013):88-96.
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