Huichen Zhao1, Shengxia Lu2, Jiachao Chai3, Yuchao Zhang1, Xiaoli Ma1, Jicui Chen4, Qingbo Guan5, Meiyan Wan6, Yuantao Liu7. 1. Department of Endocrinology, Qingdao Municipal Hospital, 5 Donghai Street, Qingdao 266071, Shandong, China. 2. Department of Cardiology, Shandong Electric Power Central Hospital, 117 Jingshi Street, Jinan, China. 3. Department of Pediatric Surgery, Women and Children's Hospital of Qingdao, 6 Tongfu Street, Qingdao 266011, Shandong, China. 4. Department of Cell Biology, Shandong University School of Medicine, 44 Wenhua Rd. West, Jinan, 250012, Shandong, China. 5. Department of Endocrinology, Provincial Hospital affiliated to Shandong University, 250021, Shandong, China. Electronic address: guanqingbo@medmail.com.cn. 6. Department of Nephrology, Qingdao Municipal Hospital, 5 Donghai Street, Qingdao 266071, Shandong, China. Electronic address: wanmeiyan07@163.com. 7. Department of Endocrinology, Qingdao Municipal Hospital, 5 Donghai Street, Qingdao 266071, Shandong, China. Electronic address: sduliuyuantao@163.com.
Abstract
BACKGROUND: The proposed mechanisms of impaired wound healing in diabetes involve sustained inflammation, excess oxidative stress and compromised agiogenesis. Hydrogen sulfide (H2S) has been reported to have multiple biological activities. We aim to investigate the role of H2S in impaired wound healing in ob/ob mice and explore the possible mechanisms involved. PROCEDURES: Full-thickness skin dorsal wounds were created on ob/ob mice and C57BL/6 mice. Cystathionine-γ-lyase (CSE) expression and H2S production were determined in granulation tissues of the wounds. Effects of NaHS on wound healing were evaluated. Inflammation and angiogenesis in granulation tissues of the wounds were examined. RESULTS: CSE expression, and H2S content were significantly reduced in granulation tissues of wounds in ob/ob mice compared with control mice. NaHS treatment significantly improved wound healing in ob/ob mice, which was associated with reduced neutrophil and macrophage infiltration, decreased production of tumor necrosis factor (TNF)-α, interleukin (IL)-6. NaHS treatment decreased metalloproteinase (MMP)-9, whereas increased collagen deposition and vascular-like structures in granulation tissues of wounds in ob/ob mice. CONCLUSION: CSE down-regulation may play a role in the pathogenesis of diabetic impaired wound healing. Exogenous H2S could be a potential agent to improve diabetic impaired wound healing by attenuating inflammation and increasing angiogenesis.
BACKGROUND: The proposed mechanisms of impaired wound healing in diabetes involve sustained inflammation, excess oxidative stress and compromised agiogenesis. Hydrogen sulfide (H2S) has been reported to have multiple biological activities. We aim to investigate the role of H2S in impaired wound healing in ob/ob mice and explore the possible mechanisms involved. PROCEDURES: Full-thickness skin dorsal wounds were created on ob/ob mice and C57BL/6 mice. Cystathionine-γ-lyase (CSE) expression and H2S production were determined in granulation tissues of the wounds. Effects of NaHS on wound healing were evaluated. Inflammation and angiogenesis in granulation tissues of the wounds were examined. RESULTS:CSE expression, and H2S content were significantly reduced in granulation tissues of wounds in ob/ob mice compared with control mice. NaHS treatment significantly improved wound healing in ob/ob mice, which was associated with reduced neutrophil and macrophage infiltration, decreased production of tumor necrosis factor (TNF)-α, interleukin (IL)-6. NaHS treatment decreased metalloproteinase (MMP)-9, whereas increased collagen deposition and vascular-like structures in granulation tissues of wounds in ob/ob mice. CONCLUSION:CSE down-regulation may play a role in the pathogenesis of diabetic impaired wound healing. Exogenous H2S could be a potential agent to improve diabetic impaired wound healing by attenuating inflammation and increasing angiogenesis.
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