Frondoza C, Jones L, Rose N R, Hatakeyama A, Phelps R, Bona C
Johns Hopkins Dept. of Orthopaedic Surgery, USA.
Curr Top Microbiol Immunol. 1996;210:299-306. doi: 10.1007/978-3-642-85226-8_31.
The possible role of silicone in the pathogenesis of a scleroderma-like syndrome is still unresolved. It has been proposed that silicone escaping from breast implants potentiates the progression of the disease. To clarify whether silicone enhances development of fibrotic skin lesions and autoantibodies, we tested its effect on tight skin (TSK/+) mice. TSK/+ mice spontaneously develop skin fibrosis and characteristic autoantibodies which resemble human scleroderma. The results of the present study indicate that silicone administration does not enhance development of skin fibrosis nor synthesis of autoantibodies to RNA polymerase and topoisomerase in TSK/+ mice.
硅酮在硬皮病样综合征发病机制中的可能作用仍未明确。有人提出，从乳房植入物中逸出的硅酮会促进疾病进展。为了阐明硅酮是否会增强纤维化皮肤病变和自身抗体的产生，我们测试了其对紧皮（TSK/+）小鼠的影响。TSK/+小鼠会自发出现皮肤纤维化和类似于人类硬皮病的特征性自身抗体。本研究结果表明，给TSK/+小鼠施用硅酮并不会增强皮肤纤维化的发展，也不会增强针对RNA聚合酶和拓扑异构酶的自身抗体的合成。
