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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
EN
Introduction and aim. Tumour necrosis factor-alpha (TNF-α) belongs to the cytokine family TNF/TNFR. As a multifunctional cytokine, TNF-α plays a significant role in diverse and a variety of cellular events such as cell survival, proliferation, differentiation, and death. As a pro-inflammatory cytokine, TNF-α acts as a bridge between inflammation and carcinogenesis. Receptor for advanced glycation end products (RAGE) are cellular receptors belonging to the immunoglobulin superfamily. As one of the primary mediators of innate immunity, acute and chronic inflammatory disorders, and certain cancers, RAGE signaling plays an important role. The aim of the present study is to analyze the prognostic significance of salivary TNF-α and RAGE in oral squamous cell carcinoma. Material and methods. A study was conducted testing saliva samples collected from ten patients with well-differentiated and moderately differentiated oral squamous cell carcinomas. To determine the levels of TNF-α and RAGE in unstimulated saliva from patients, an ELISA kit from RAY BIOTECH was used for the study, and the readings were read at 450 nm. Statistical analysis was performed using SPSS software. Version 23 of SPSS was used to plot the standard curve. Statistical comparisons were done using Mann-Whitney U test and ROC analysis. Results. Salivary TNF-α and RAGE in patients were considered to be induced by radiotherapy at a higher level in moderately differentiated squamous cell carcinoma when compared to well differentiated squamous cell carcinoma. Thus, there is an increase in the induced Salivary TNF-α and RAGE levels by radiotherapy with increase in the histological stages of oral squamous cell carcinoma. The statistical analysis also proved the same. Conclusion. Hence salivary TNF-α and RAGE may be used as a biomarker for oral cancer to predict the prognosis.
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