- Tytuł:
- Subcutaneous administration of infliximab-attenuated silica-induced lung fibrosis
- Autorzy:
-
Zhang, Hua
Sui, Jun-Na
Gao, Lei
Guo, Jian - Powiązania:
- https://bibliotekanauki.pl/articles/2162006.pdf
- Data publikacji:
- 2018-07-04
- Wydawca:
- Instytut Medycyny Pracy im. prof. dra Jerzego Nofera w Łodzi
- Tematy:
-
infliximab
silicosis
TNF-α
rat model
NF-κB
iNOS - Opis:
- 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
- Źródło:
-
International Journal of Occupational Medicine and Environmental Health; 2018, 31, 4; 503-515
1232-1087
1896-494X - Pojawia się w:
- International Journal of Occupational Medicine and Environmental Health
- Dostawca treści:
- Biblioteka Nauki
Artykuł