Radley Hannah G, Davies Marilyn J, Grounds Miranda D
School of Anatomy and Human Biology, The University of Western Australia, Anatomy and Human Biology, Perth, WA 6009, Australia.
Neuromuscul Disord. 2008 Mar;18(3):227-38. doi: 10.1016/j.nmd.2007.11.002. Epub 2008 Jan 22.
Tumour necrosis factor (TNF) is a potent inflammatory cytokine that appears to exacerbate damage of dystrophic muscle in vivo. The monoclonal murine specific antibody cV1q that specifically neutralises murine TNF demonstrated significant anti-inflammatory effects in dystrophic mdx mice. cV1q administration protected dystrophic skeletal myofibres against necrosis in both young and adult mdx mice and in adult mdx mice subjected to 48 h voluntary wheel exercise. Long-term studies (up to 90 days) in voluntarily exercised mdx mice showed beneficial effects of cV1q treatment with reduced histological evidence of myofibre damage and a striking decrease in serum creatine kinase levels. However, in the absence of exercise long-term cV1q treatment did not reduce necrosis or background pathology in mdx mice. An additional measure of well-being in the cV1q treated mice was that they ran significantly more than control mdx mice.
肿瘤坏死因子（TNF）是一种强效的炎性细胞因子，似乎会加剧体内营养不良性肌肉的损伤。特异性中和小鼠TNF的单克隆鼠源特异性抗体cV1q在营养不良的mdx小鼠中表现出显著的抗炎作用。给予cV1q可保护营养不良的骨骼肌纤维在幼年和成年mdx小鼠以及进行48小时自愿轮转运动的成年mdx小鼠中免于坏死。对自愿运动的mdx小鼠进行的长期研究（长达90天）表明，cV1q治疗具有有益效果，肌纤维损伤的组织学证据减少，血清肌酸激酶水平显著降低。然而，在缺乏运动的情况下，长期给予cV1q并不能减少mdx小鼠的坏死或背景病理。cV1q治疗小鼠的另一个健康指标是它们的奔跑距离明显超过对照mdx小鼠。
