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Ganoderma lucidum Polysaccharide Accelerates Refractory Wound Healing by Inhibition of Mitochondrial Oxidative Stress in Diabetes
Author(s) -
Tie Lu,
Lin ZhiBin,
Li XueJun
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.lb559
Subject(s) - wound healing , oxidative stress , nitrotyrosine , pharmacology , antioxidant , superoxide dismutase , granulation tissue , diabetes mellitus , glutathione peroxidase , medicine , streptozotocin , chemistry , biochemistry , endocrinology , enzyme , surgery , nitric oxide synthase
Background Impaired wound healing in diabetic patients is a serious complication with limited treatment regimens. Gene therapy of mitochondrial antioxidant enzyme manganese superoxide dismutase (MnSOD) was able to restore diabetic wound healing with suppression of O 2 .− . The present study was designed to determine protective effects of Ganoderma lucidum polysaccharide ( Gl ‐PS), as a potent inducer of MnSOD, on diabetic wound healing. Method and Results Streptozotocin‐induced diabetic mice with full‐thickness excisional wounds were administered with Gl ‐PS (10, 50 or 250 mg/kg/day, i.g.). Gl ‐PS dose‐dependently rescued the delay of wound closure and increased the mean perfusion rate around the wound in diabetic mice. Diabetic conditions markly increased mitochondrial O 2 .− production and nitrotyrosine formation in wound tissues, which were normalized with Gl ‐PS treatment. In diabetic wound tissues, the protein level of 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 in diabetic mice skin. Conclusion Gl ‐PS rescued the delayed wound healing and improved wound angiogenesis in diabetic mice, at least in part, by suppression of mitochondrial oxidative stress. This work was supported by the National Natural Science Foundation of China.