Rosenberg N L
Research Division, Veterans Administration Medical Center, Denver, CO 80220.
Arthritis Rheum. 1988 Jun;31(6):806-11. doi: 10.1002/art.1780310619.
Skeletal muscle from (New Zealand black x New Zealand white)F1 and MRL-lpr/lpr mice was examined for histopathologic abnormalities. Although young animals had no muscle abnormalities, older mice in both strains had the following histopathologic abnormalities: perimysial/endomysial inflammation, acute simple denervation, muscle degeneration/necrosis, and an increase in internal nuclei. MRL-lpr/lpr mice had the following additional histopathologic abnormalities: inflammatory vascular disease (vasculitis), central myofibrillar loss, fascial inflammation, and tubular aggregates. These abnormalities are comparable with those seen in human connective tissue diseases, particularly the association with inflammation. These mouse strains provide good animal models for the study of immunopathologic processes of skeletal muscle associated with connective tissue disease.
对（新西兰黑鼠×新西兰白鼠）F1代小鼠和MRL-lpr/lpr小鼠的骨骼肌进行了组织病理学异常检查。尽管幼年动物没有肌肉异常，但两个品系的老年小鼠都有以下组织病理学异常：肌束膜/肌内膜炎症、急性单纯性去神经、肌肉变性/坏死以及肌核内移增加。MRL-lpr/lpr小鼠还有以下额外的组织病理学异常：炎症性血管疾病（血管炎）、中央肌原纤维缺失、筋膜炎症和管状聚集物。这些异常与人类结缔组织疾病中所见的异常相当，特别是与炎症的关联。这些小鼠品系为研究与结缔组织疾病相关的骨骼肌免疫病理过程提供了良好的动物模型。
