Oda Hiroshi, Matsuzaki Hiromi, Tokuhashi Yasuaki, Wakabayashi Ken, Uematsu Yoshinao, Iwahashi Masaki
Department of Orthopaedic Surgery, Nihon University Hospital, 30-1 Oyaguchi-Kamimachi, Itabashi-ku, Tokyo 173-8610, Japan.
J Orthop Sci. 2004;9(2):135-41. doi: 10.1007/s00776-003-0759-y.
We have investigated the intervertebral discs of rat-smoking models to demonstrate that smoking is a cause of degenerative intervertebral disc disease. A smoking box was developed for this study. We exposed 8-week-old rats to indirect tobacco smoke inhalation. Each rat was forced to inhale the smoke from one cigarette per hour. The mean blood nicotine level of rodents exposed to cigarette smoke corresponds to about twice that of ordinary human smokers. Histological and immunological studies were then performed to assess the effects of smoking for varying periods of time. After 8 weeks, the chondrocytes in the disordered annulus fibrosus layer tended to grow larger and attain a rounder form than normal chondrocytes. The interleukin-1beta level in the 8-week smoking group was significantly higher than that of the control group. Tobacco smoke inhalation increased local production and release of inflammatory cytokines and resultant decomposition of chondrocyte activity.
我们对大鼠吸烟模型的椎间盘进行了研究，以证明吸烟是退行性椎间盘疾病的一个病因。为此研究开发了一个吸烟箱。我们让8周龄的大鼠间接吸入烟草烟雾。每只大鼠每小时被迫吸入一支香烟的烟雾。暴露于香烟烟雾中的啮齿动物的平均血液尼古丁水平约为普通人类吸烟者的两倍。然后进行组织学和免疫学研究，以评估不同时间段吸烟的影响。8周后，紊乱的纤维环层中的软骨细胞往往比正常软骨细胞长得更大且呈更圆的形态。8周吸烟组中的白细胞介素-1β水平显著高于对照组。吸入烟草烟雾增加了炎症细胞因子的局部产生和释放以及软骨细胞活性的分解。
