Effect of NF-κB inhibitor on high-mobility group protein B1 expression in a COPD rat model

Abstract

The aim of the present study was to investigate the effect of the nuclear factor‑κB (NF‑κB) inhibitor, pyrrolidine dithiocarbamate (PDTC), on high‑mobility group protein B1 (HMGB1) expression in a rat model of chronic obstructive pulmonary disease (COPD). The COPD model was developed by administering lipopolysaccharides to the airways of rats and smudging (group B). In addition, a model of COPD complicated with hypoxia was established by administering lipopolysaccharides to the airways of rats, smudging and hypoxia (group C). PDTC was administered to the treatment groups by intraperitoneal injection. Reverse transcription polymerase chain reaction (RT‑PCR) and western blot analysis were used to detect the expression of HMGB1 and NF‑κB in lung tissue. RT‑PCR and western blot analysis demonstrated that HMGB1 mRNA and protein expression in groups B and C increased significantly (P<0.05) compared with control group A. In addition, HMGB1 expression in groups B and C gradually increased. HMGB1 mRNA and protein expression in groups B1 and C1 decreased (P<0.05) compared with B and C. NF‑κB protein expression in groups B and C increased significantly (P<0.05) compared with A. NF‑κB protein expression in groups B1 and C1 decreased compared with B and C. Therefore, HMGB1 mRNA and protein expression was identified to be positively correlated with NF‑κB protein expression. The NF‑κB inhibitor, PDTC, was demonstrated to significantly inhibit HMGB1 expression in lung tissues of rats with COPD and this mechanism may be associated with the NF‑κB signal transduction pathway.