目的：通过球结膜下注射基质金属蛋白酶(metalloproteinase,MMP)-1、3构建结膜松弛症的动物模型。方法：20只新西兰大白兔随机分为4组：对照组无干预措施；伪造模组球结膜下注射生理盐水；MMP-1组球结膜下注射MMP-1；MMP-3组球结膜下注射MMP-3。8周后观察眼前节照相和眼前节光学相干检查、泪液蕨类试验及结膜组织光镜检查结果。结果：对照组和伪造模组未见结膜皱褶形成，泪液羊齿状结晶样结构完整，光镜下未见胶原和弹力纤维破坏；MMP-1组可见结膜皱褶形成，泪液羊齿状结晶样结构破坏，光镜下见胶原和弹力纤维破坏；MMP-3组未见结膜皱褶形成，泪液羊齿状结晶样结构部分破坏，光镜下见胶原和弹力纤维部分破坏。结论：球结膜下注射MMP-1可构建结膜松弛症1~2级的动物模型。
Objective:To establish an animal model of conjunctivochalasis by subconjunctival injection of matrix metalloproteinase 1 and 3. Methods:New Zealand white rabbits were randomly divided into four groups, the control group had no intervention measures; Pseudo model group was injected susbconjunctival with normal saline; MMP-1 group was injected subconjunctival with matrix metalloproteinase 1; MMP-3 group was injected subconjunctival with matrix metalloproteinase 3. Afer 8 weeks, the results of anterior segment photography and optical coherence test, tear fern test and conjunctival tissue light microscopy were observed. Results:No conjunctival folds were observed in the control group and Pseudo model group, the lacrimal fern-shaped crystalline structures were intact, and no destruction of collagen and elastic fbers was found under the light microscope. In MMP-1 group, conjunctival folds were formed, lacrimal ferns crystalline structures were damaged, and collagen and elastic fbers were damaged under light microscope. No conjunctival folds were found in MMP-3 group, and the lacrimal ferns crystalline structure was partially destroyed, while the collagen and elastic fibers were partially destroyed under light microscope. Conclusion:Subconjunctival injection of matrix metalloproteinase-1 can construct the animal model of conjunctivochalasis of 1-2 grades.
视神经脊髓炎谱系疾病(neuromyelitis optica spectrum disorders，NMOSD)是一种中枢神经系统炎性脱髓鞘性疾病，以视神经、脊髓和大脑受累为主要特征，该疾病易复发且致盲、致残率高，严重威胁人类视力和健康。目前NMOSD病因尚不明确，现有治疗方案也无法彻底治愈NMOSD，而动物模型是探索其发病机制与病理生理特点的重要工具。NMOSD动物模型主要建立在抗水通道蛋白4抗体(anti-aquaporin 4 immunoglobulin G，AQP4-IgG)致病基础上，主要包括破坏或绕过血脑屏障(blood brain barrier，BBB)被动转移AQP4-IgG或AQP4特异性T细胞等，目前还没有一种动物模型可以完整模拟人类NMOSD的临床和病理特征，因此在研究中选择合适的动物模型对相关研究至关重要。
Neuromyelitis optica spectrum disorders (NMOSD) is an inflammatory demyelinating disease of the central nervous system. It is mainly characterized by the involvement of the optic nerve, spinal cord and brain. The disease is prone to relapse and has a high rate of blindness and disability, which seriously threatens human vision and health. At present, the etiology of NMSOD is not clear, and the existing treatment schemes can’t completely cure NMOSD. Animal models are important tools to explore its pathogenesis and pathophysiological characteristics. NMOSD animals were mainly established on the basis of anti-aquaporin 4 immunoglobulin G (AQP4-IgG), including destroying or bypassing the blood-brain barrier and passively transferring AQP4-IgG or AQP4 specific T cells. At present, no animal model can completely simulate the clinical and pathological characteristics of human NMOSD. Therefore, it is important to select appropriate animal models for the study. This article reviews various animal models of NMOSD in recent years, and discusses the advantages and disadvantages of various models, in order to provide references for the study of the progress and treatment of NMOSD.
