首页    期刊浏览 2024年11月29日 星期五
登录注册

文章基本信息

  • 标题:Subcutaneous administration of infliximab-attenuated silica-induced lung fibrosis
  • 本地全文:下载
  • 作者:Hua Zhang ; Hua Zhang ; Jun-Na Sui
  • 期刊名称:International Journal of Occupational Medicine and Environmental Health
  • 印刷版ISSN:1232-1087
  • 电子版ISSN:1896-494X
  • 出版年度:2018
  • 卷号:31
  • 期号:4
  • 页码:503-515
  • DOI:10.13075/ijomeh.1896.01037
  • 语种:English
  • 出版社:Walter de Gruyter GmbH
  • 摘要:Objectives To investigate the influence of the anti-tumor necrosis factor-α infliximab (IFX) in the case of rats with silicosis. Material and Methods Forty-eight Wistar rats were randomly divided into 3 groups. The study group (N = 16) – silicosis was induced by intratracheal instillation of 50 mg silica on day 1, and IFX was subcutaneously administered at a dose of 15 mg/kg of body weight from day 2 to day 6, the vehicle group (N = 16) – silica used as the study group but without IFX, the sham group (N = 16) – 1 ml of saline was intratracheal-used. Eight rats in each group were euthanized on day 7 and on day 14, respectively. Lung tissue sections were stained with hematoxylin and eosin or Masson’s trichromedye. The nuclear factor-κB p65 (NF-κB p65) positioning in the lung tissues were determined by immunohistochemical staining. Levels of tumor necrosis factor α (TNF-α) in rat serum and bronchoalveolar lavage fluid were measured with enzyme linked immunosorbent assay. The inducible nitric oxide synthase (iNOS) mRNA in the lung tissues was measured by quantitative real-time polymerase chain reaction, as well as inhibitor protein-κB (I-κB) and NF-κB p65 expression were measured quantitatively by western blotting. Results Silica installation increased the lung tissues inflammation reaction, oxidative stress and pulmonary fibrosis. Infliximab treatment significantly improved silica-induced lung pathological changes (inflammatory cells, collagen deposition), decreased the TNF-α inhibited NF-κB signaling (I-κB, NF-κB p65) as well as oxidant status (iNOS). Conclusions Infliximab may improve silica-induced pulmonary inflammation by decreasing the TNF-α, inhibiting NF-κB signaling (I-κB, NF-κB p65) as well as oxidant status (iNOS), which suggest that IFX has potential role in the treatment of silica-induced lung damage. Int J Occup Med Environ Health 2018;31(4):503–515
国家哲学社会科学文献中心版权所有