Nagatomo Hiroko, Morimoto Yasuo, Oyabu Takako, Hirohashi Masami, Ogami Akira, Yamato Hiroshi, Kuroda Kaori, Higashi Toshiaki, Tanaka Isamu
Department of Occupational Pneumology, Institute of Industrial and Ecological Sciences, University of Occupational and Environmental Health, Kitayushu, Japan.
J Occup Health. 2006 Mar;48(2):124-8. doi: 10.1539/joh.48.124.
Oxidative stress is thought to be the pathogenesis of pulmonary fibrosis induced by particles, and heme oxygenase-1 (HO-1) protects lung tissue against oxidative stress. We hypothesized that HO-1 is also associated with oxidative lung injury caused by exposure to particles. The present study was conducted to investigate the time course of HO-1 expression of lungs exposed to crystalline silica in vivo. Male Wistar rats were administered 1 mg or 2 mg of crystalline silica suspended in saline by a single intratracheal instillation and were sacrificed at 3 d, 1 wk, 1 month, 3 months and 6 months of recovery time. The expression of HO-1 was observed by western blot analysis and immunostaining. Protein levels of HO-1 were increased compared to the controls at 3 d, and from 1 month to 6 months following intratracheal instillation of 2 mg of crystalline silica. The levels of HO-1 were increased compared to the controls from 1 month to 6 months following intratracheal instillation of 1 mg of crystalline silica. Many HO-1 positive cells were found particularly in the alveolar macrophages during immunostaining. These findings suggest that HO-1 is related to lung injury arising from exposure to crystalline silica.
氧化应激被认为是颗粒诱导的肺纤维化的发病机制，而血红素加氧酶-1（HO-1）可保护肺组织免受氧化应激的影响。我们推测HO-1也与接触颗粒引起的氧化性肺损伤有关。本研究旨在调查体内暴露于结晶二氧化硅的肺组织中HO-1表达的时间进程。通过单次气管内滴注，给雄性Wistar大鼠施用1毫克或2毫克悬浮于盐水中的结晶二氧化硅，并在恢复时间的3天、1周、1个月、3个月和6个月时处死。通过蛋白质印迹分析和免疫染色观察HO-1的表达。与对照组相比，在气管内滴注2毫克结晶二氧化硅后的3天以及1个月至6个月时，HO-1的蛋白质水平升高。与对照组相比，在气管内滴注1毫克结晶二氧化硅后的1个月至6个月时，HO-1的水平升高。在免疫染色过程中，尤其在肺泡巨噬细胞中发现了许多HO-1阳性细胞。这些发现表明HO-1与接触结晶二氧化硅引起的肺损伤有关。
