期刊
CELLULAR PHYSIOLOGY AND BIOCHEMISTRY
卷 29, 期 3-4, 页码 583-594出版社
KARGER
DOI: 10.1159/000338512
关键词
Ganoderma lucidum polysaccharide (Gl-PS); Oxidative stress; Mitochondria; Diabetes; Manganese superoxide dismutase (MnSOD); p66Shc; Nitrotyrosine
资金
- National Natural Science Foundation of China [30901803, 91129727, 81020108031, 30973558, 30572202, 30901815]
- Research Fund for the Doctoral Program of Higher Education of China [20090001120046]
- Ministry of Science and Technology in China [2009ZX09103-144]
- Ministry of Education of China [B07001]
Background/Aims. 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 Ganoderma lucidum polysaccharide (Gl-PS) on diabetic wound healing and investigate underlying mechanisms. Methods. Streptozotocin (STZ)-induced type 1 diabetic mice with full-thickness excisional wounds were intragastrically administered with 10, 50 or 250 mg/kg/day of Gl-PS. Results. Gl-PS dose-dependently rescued the delay of wound closure in diabetic mice. 50 and 250 mg/kg/day of Gl-PS treatment significantly increased the mean perfusion rate around the wound in diabetic mice. Diabetic conditions markly increased mitochondrial superoxide anion (O-2(center dot-)) production, nitrotyrosine formation, and inducible nitric oxide synthase (iNOS) activity in wound tissues, which were normalized with Gl-PS treatment. In diabetic wound tissues, the protein level of manganese superoxide dismutase (MnSOD) was unchanged whereas MnSOD activity was inhibited and its nitration was potentiated; Gl-PS administration suppressed MnSOD nitration and increased MnSOD and glutathione peroxidase (GPx) activities. Moreover, Gl-PS attenuated the redox enzyme p66Shc expression and phosphorylation dose-dependently in diabetic mice skin. Conclusion. Gl-PS rescued the delayed wound healing and improved wound angiogenesis in STZ-induced type 1 diabetic mice, at least in part, by suppression of cutaneous MnSOD nitration, p66Shc and mitochondrial oxidative stress. Copyright (C) 2012 S. Karger AG, Basel
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