作者机构：
[陈诚; 黄炎; 夏萍萍; 张帆; 叶治; 李龙艳] Department of Anesthesiology, Affiliated Xiangya Hospital of Central South University, Changsha, 410078, China;[刘宇] Department of Anesthesiology, The First Affiliated Hospital of University of South China, Hengyang, 421001, China
通讯机构：
[Ye, Z.] D;Department of Anesthesiology, China
作者机构：
[张益玮; 肖帅; 彭秀达] Department of Hepatobiliary and Pancreatic Surgery, Gastrointestinal Surgery, Institute of Clinical Medicine, The First Affiliated Hospital, University of South China, Hengyang, 421001, China
通讯机构：
[Xiao, S.] D;Department of Hepatobiliary and Pancreatic Surgery, China
作者机构：
南华大学药学与药理学研究所,湖南省高校药物蛋白质组学重点实验室,湖南衡阳421001;南华大学肿瘤研究所,湖南省胃癌研究中心,湖南省高校肿瘤细胞与分子病理学重点实验室,湖南衡阳421001;湖南省中医药专科学校附属医院肿瘤科,湖南株洲412012;[丁恩] Cancer Research Institute, Center for Gastric Cancer Research of Hunan Province, Key Lab of Cancer Cellular, Molecular Pathology of Hunan Provincial University, University of South China, Hunan, Hengyang, 421001, China, Dept of Oncology, The Affiliated Hospital, Hunan College of Traditional Chinese Medicine, Hunan, Zhuzhou, 412012, China;[苏波] Institute of Pharmacy and Pharmacology, Key Lab for Pharmacoproteomics, Hunan Provincial University, University of South China, Hunan, Hengyang, 421001, China, Cancer Research Institute, Center for Gastric Cancer Research of Hunan Province, Key Lab of Cancer Cellular, Molecular Pathology of Hunan Provincial University, University of South China, Hunan, Hengyang, 421001, China
作者机构：
[蒋素素; 龙石银; Shao J.-Q.; 张敏; 田英; 张彩平; 袁育林; 李博洁; 王楚瑶] Dept of Biochemistry & Molecular Biology, Medical College, University of South China, Hunan, Hengyang, 421001, China;[向德彪; 廖端芳] School of Pharmacy, Hunan University of Chinese Medicine, Changsha, 410208, China;[贺卫和; 杨慧仙] Institute of Cardiovascular Diseases, University of South China, Hunan, Hengyang, 421001, China
作者机构：
[Chen Nai-Hong; Feng Ju-Ling] Hunan Univ Chinese Med, Coll Pharm, Changsha 410208, Peoples R China.;[Wang Zhen-Zhen; Chen Nai-Hong] Peking Union Med Coll, Neurosci Ctr, Inst Mat Med, Beijing 100050, Peoples R China.;[Wang Zhen-Zhen; Chen Nai-Hong] Chinese Acad Med Sci, Beijing 100050, Peoples R China.;[Feng Ju-Ling] Univ South China, Hengyang Med Coll, Res Lab Translat Med, Hengyang 421001, Peoples R China.;[Zhao Lei] Univ South China, Affiliated Hosp 1, Dept Gastrointestinal Surg, Hengyang 421001, Peoples R China.
通讯机构：
[Chen Nai-Hong] H;[Chen Nai-Hong] P;Hunan Univ Chinese Med, Coll Pharm, Changsha 410208, Peoples R China.;Peking Union Med Coll, Neurosci Ctr, Inst Mat Med, Beijing 100050, Peoples R China.
作者机构：
[Hong Huang] Institute of Clinical Medicine, The First Affiliated Hospital of University of South China, Hengyang 421001, China;[Kai Yin] Center for Diabetic Systems Medicine, Guangxi Key Laboratory of Excellence, The Second Affiliated Hospital of Guilin Medical University, Guilin 541199, China;[Huifang Tang] Department of Cardiology, The First Affiliated Hospital of University of South China, Hengyang 421001, China
通讯机构：
[Kai Yin] C;[Huifang Tang] D;Department of Cardiology, The First Affiliated Hospital of University of South China , Hengyang 421001, China<&wdkj&>Center for Diabetic Systems Medicine, Guangxi Key Laboratory of Excellence, The Second Affiliated Hospital of Guilin Medical University , Guilin 541199, China
摘要：
The immune system plays a vital role in restoring tissue integrity and function upon injury. Wound healing is a highly dynamic process that involves early inflammatory phase, proliferative phase, and finally the maturation phase. Tissue repair begins with the formation of granulation tissue that contains macrophages to play anti-inflammatory roles. Macrophages within the granulation tissue acquire a spectrum of phase-specific phenotypes affecting fibroblast function, including myofibroblast differentiation, myofibroblast proliferation, and extracellular matrix(ECM) remodeling [1]. Nevertheless, the underlying mechanism that macrophage contributes to the myofibroblast production during tissue repair remains largely unexplored.
作者机构：
[刘政海; 李彩; 王五洲; 曹文宇; 罗诗诗] Clinical Anatomy & Reproductive Medicine Application Institute, Medical College, University of South China, Hengyang, 421001, China;[徐杨] Department of Physiology, Medical College, University of South China, Hengyang, 421001, China;[何洁] Department of Pathology, Medical College, University of South China, Hengyang, 421001, China;[Wang W.; 何淑雅] School of Public Health, University of South China, Hengyang, 421001, China;[艾小红] Department of Radiation Oncology, The First Affiliated Hospital of University of South China, Hengyang, 421001, China
通讯机构：
[Cao, W.] C;Clinical Anatomy & Reproductive Medicine Application Institute, Medical College, University of South China, Hengyang, China
摘要：
Oxidative stress contributes to the pathogenesis of neurodegenerative diseases. With the aim to find reagents that reduce oxidative stress, a phage display library was screened for peptides mimicking α2,6-sialyllactose (6'-SL), which is known to beneficially influence neural functions. Using Sambucus nigra lectin, which specifically binds to 6'-SL, we screened a phage display library and found a peptide comprising identical sequences of 12 amino acids. Mimetic peptide, reverse peptide and scrambled peptide were tested for inhibition of 6'-SL binding to the lectin. Indeed, lectin binding to 6'-SL was inhibited by the most frequently identified mimetic peptide, but not by the reverse or scrambled peptides, showing that this peptide mimics 6'-SL. Functionally, mimetic peptide, but not the reverse or scrambled peptides, increased viability and expression of neural cell adhesion molecule L1 in SK-N-SH human neuroblastoma cells, and promoted survival and neurite outgrowth of cultured mouse cerebellar granule neurons challenged by H(2)O(2)-induced oxidative stress. The combined results indicate that the 6'-SL mimetic peptide promotes neuronal survival and neuritogenesis, thus raising hopes for the treatment of neurodegenerative diseases. This study was approved by the Medical Ethics Committee of Shantou University Medical College, China (approval No. SUMC 2014-004) on February 20, 2014.
