Subcutaneous administration of infliximab-attenuated silica-induced lung fibrosis
Hua Zhang 1,2
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Qilu Hospital of Shandong University, Jinan, China (Department of Respiratory Medicine)
Qingdao Central Hospital, Qingdao, China (Department of Occupational Disease)
Qingdao Central Hospital, Qingdao, China (Department of Clinical Laboratory)
Qingdao Blood Center, Qingdao, China (Department of Clinical Laboratory)
Online publication date: 2017-11-21
Corresponding author
Jian Guo   

Qingdao Central Hospital, Department of Clinical Laboratory, 127 Siliu Nan Road, Qingdao 260042, China
Int J Occup Med Environ Health. 2018;31(4):503-15
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
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