Subcutaneous administration of infliximab-attenuated silica-induced lung fibrosis.

Abstract:

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.

authors

Zhang H,Sui JN,Gao L,Guo J

doi

10.13075/ijomeh.1896.01037

subject

Has Abstract

pub_date

2018-07-04 00:00:00

pages

503-515

issue

4

eissn

1232-1087

issn

1896-494X

pii

77973

journal_volume

31

pub_type

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