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2017 | 31 | 4 | 503-515

Article title

Subcutaneous administration of infliximab-attenuated silica-induced lung fibrosis

Content

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Abstracts

EN
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

Keywords

Year

Volume

31

Issue

4

Pages

503-515

Physical description

Dates

published
2018

Contributors

author
  • Qilu Hospital of Shandong University, Jinan, China (Department of Respiratory Medicine)
  • Qingdao Central Hospital, Qingdao, China (Department of Occupational Disease)
author
  • Qingdao Central Hospital, Qingdao, China (Department of Clinical Laboratory)
author
  • Qingdao Blood Center, Qingdao, China (Department of Clinical Laboratory)
author
  • Qingdao Central Hospital, Qingdao, China (Department of Clinical Laboratory)

References

Document Type

Publication order reference

Identifiers

Biblioteka Nauki
2162006

YADDA identifier

bwmeta1.element.ojs-doi-10_13075_ijomeh_1896_01037
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