WANG Kai, LIU Zhi-hong, WANG He-jing, WANG Yao, WEI Cong-hui, ZHANG Na, ZHOU Ci. Beryllium Oxide-Induced Pulmonary Fibrosis in Rats and Dynamic Changes of Related Indicators[J]. Journal of Environmental and Occupational Medicine, 2016, 33(7): 644-649. DOI: 10.13213/j.cnki.jeom.2016.16240
Citation: WANG Kai, LIU Zhi-hong, WANG He-jing, WANG Yao, WEI Cong-hui, ZHANG Na, ZHOU Ci. Beryllium Oxide-Induced Pulmonary Fibrosis in Rats and Dynamic Changes of Related Indicators[J]. Journal of Environmental and Occupational Medicine, 2016, 33(7): 644-649. DOI: 10.13213/j.cnki.jeom.2016.16240

Beryllium Oxide-Induced Pulmonary Fibrosis in Rats and Dynamic Changes of Related Indicators

  • Objective To study the pulmonary pathological changes and test dynamic changes of lung fibrosis related indicators of SD rats with pulmonary fibrosis induced by beryllium oxide(BeO).
    Methods Sixty-four specific pathogen free SD male rats were randomly divided into a negative control group and a BeO exposure group. Using disposable non-exposed intratracheal instillation, the BeO group was injected with 10 g/L BeO(0.5 mL), and the negative control group was injected with 0.9% saline at the same volume. The two groups of rats were respectively neutralized at 20, 40, 60, and 80 d after exposure, eight rats in every batch and each group. Lung tissue specimens were prepared to observe pathological changes under optical microscope and test expression of collagen I(COL-Ⅰ), collagen III(COL-Ⅲ), α-smooth muscle actin(α-SMA), and transforming growth factor β1(TGF-β1) in lung tissue homogenate and serum.
    Results The early pathological changes in lung tissue of the BeO group were located in bronchus, displaying interstitial infiltration of monocytes/macrophages and thickened alveolar septum; while in late stage, it showed obviously thickened alveolar septum, narrowed alveolar space, some alveolus missing and disordered, fibrosis nodules, and BeO dust in the center of nodules, indicating consolidation in part of lung tissues. In the lung tissue homogenate, compared with the negative control group, the COL-Ⅰexpression level in the exposed group was higher at the same time points(P < 0.05); the COL-Ⅲ in the exposed group was higher at 60d and 80d(P < 0.05); the α-SMA in the exposed group was higher at 80d(P < 0.05); the TGF-β1 in the exposed group was higher at 60 d and 80 d(P < 0.05). Compared with 20 d, there were no significant differences in all indices at other time points of the negative control group; the COL-Ⅰin the exposed group at 40 d, 60 d, and 80 d was higher(P < 0.05); the α-SMA, COL-Ⅲ, and TGF-β1 in the exposed group at 80 d were higher(P < 0.05). In serum, compared with the negative control group, the COL-Ⅲ and TGF-β1 in the exposed group were higher at 60 d and 80 d(P < 0.05); the COL-Ⅰin the exposed groups was higher at 80 d(P < 0.05); the α-SMA in the exposed group was higher at the same time points(P < 0.05). Compared with 20 d, there were no significant differences in all indices at other time points of the negative control group; the COL-Ⅲ in the exposure group was higher at 60 d and 80 d(P < 0.05); the COL-Ⅰand TGF-β1 in the exposure group were higher at 80 d(P < 0.05).
    Conclusion BeO exposure causes lung fibrosis in rats, and COL-Ⅰ, COL-Ⅲ, α-SMA, and TGF-β1 expression levels are increased at different time points.
  • loading

Catalog

    /

    DownLoad:  Full-Size Img  PowerPoint
    Return
    Return