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腺苷A2A受体基因敲除小鼠瘢痕胶原亚型的变化
作者姓名:肖 虎  李少华  王德昌  霍 然  王一兵  冯永强  李 强
作者单位:山东大学附属省立医院烧伤整形科,山东省济南市 250021
基金项目:山东省科技厅优秀中青年科学家奖励基金(BS2009YY043);山东省卫生厅医药卫生科技发展计划项目(2009QZ023)。
摘    要:背景:作者前期研究发现腺苷受体激动剂可以刺激胶原合成,腺苷受体拮抗剂可以抑制胶原合成,并且可以减轻皮肤胶原纤维增生。腺苷A2A 受体基因敲除小鼠瘢痕转化生长因子β表达降低。 目的:利用苦味酸-天狼星红偏振光法观察腺苷A2A 受体基因敲除小鼠瘢痕胶原亚型的变化并探讨其机制。 方法:腺苷A2A受体基因敲除小鼠和野生型小鼠制作瘢痕模型,采用苦味酸-天狼星红偏振光法对瘢痕组织中胶原的性质及分布特点进行观察、确定瘢痕组织胶原类型、分布、排列与水平。 结果与结论:偏振光显微镜下可见野生型组小鼠增生性瘢痕组织中含有大量的嗜酸性胶原蛋白纤维束,Ⅰ型胶原纤维为红色,呈致密的条束状,显示很强的双折光性,腺苷A2A 受体基因敲除小鼠瘢痕缺乏粗大胶原束,呈稀疏的条束状,排列相对整齐、密度较为均匀,Ⅰ型胶原纤维水平减少(P < 0.01),瘢痕增生显著减轻。提示腺苷A2A 受体参与瘢痕增生,对预防瘢痕增生有积极意义。

关 键 词:腺苷  腺苷受体  瘢痕  苦味酸-天狼猩红偏振光法  胶原  
收稿时间:2011-07-16

Detection of collagens in hypertrophic scars of adenosine receptor A2A knockout mice bypicrosirius polarization method
Authors:Xiao Hu  Li Shao-hua  Wang De-chang  Huo Ran  Wang Yi-bing  Feng Yong-qiang  Li Qiang
Institution:Department of Burnsand Plastic Surgery,Provincial HospitalAffiliated toShandong University,Jinan 250021,Shandong Province,China
Abstract:BACKGROUND:Recent study shows that the adenosine receptor agonists can promote the collagen synthesis, and theadenosine receptor antagonists can inhibit the collagen synthesis and reduce the proliferation of skin collagen fiber. Theexpression of transforming growth factor β (TGF-β) in hypertrophic scar of adenosine A2A knockout mice models is decreased. OBJECTIVE:To observe the changes of collagens in hypertrophic scars of adenosine receptor A2A knockout mice and itsmechanism by picric acid-sirius red polarization method. METHODS:The models of hypertrophic scars were made by adenosine A2A knockout mice and wild-type mice. The characterand the distribution of the collagen in the hypertrophic scars were observed by picric acid-sirius red polarization method, and thetype of the collagen, distribution, arrangement and content was confirmed. RESULTS AND CONCLUSION:A large amount of eosinophilic collagen protein fibers were observed under polarizingmicroscope in the hypertrophic scars of wild-type control group. Type Ⅰ collagen fibers were in red and compact bunchiness andexhibited strong double refraction, the hypertrophic scars of adenosine A2A knockout mice were lack of thick collagen bundlesand was in sparse bunchiness, and the collage bundles were well-arranged and well-distributed. Compared with the wild-typecontrol group, adenosine A2A knockout mice showed significantly lower typeⅠcollagen fibers level (P < 0.01), as well as thehypertrophic scars. It indicated that adenosine A2A receptors played an active role in the proliferation of scars and could preventthe proliferation of scars.
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