Effects of NF-κB inhibitor on nuclear factor-κB and intercellular adhesion moceule-1 in lung injury associated with radiation of rats / 中华劳动卫生职业病杂志

ABSTRACT

Objective@#To investigate the mechanism of lung injury caused by radiation-induced lung injury by observing the change of nuclear factor (NF-κB) and intercellular adhesion moceule-1 (ICAM-1) in rats and the effects of pyrrolidine dithiocarbamate (PDTC) .@*Methods@#80 SD female rats were randomly classified into 4 groups control group, radiation group, PDTC treatment group and PDTC group.The radiation induced pulmonary injury model was preformed by using 6 MV X-rays to deliver 8 Gy per day for 5 consecutive days with 40 Gy in total to the thorax of each animal.PDTC was given from 3 d before radiation to 30 d after the first radiation. Rats in control group and PDTC group received the same dose of saline. Animals were sacrificed at 8 week and 24 week after radiation, respectively. The lungs were removed and processed for HE and Masson staining, hydroxyproline content measurement, and real-time quantitative reverse transcription-polymerase chain (RT-PCR) ICAM-1mRNA and NF-κB p65mRNA were detected, Statistical analysis were carried out.@*Results@#Compared with radiation group, there was an obvious amelioration in pathological injury of lung tissue in PDTC treatment group. The lung coefficient and the content of Hyp in PDTC treatment group were significantly lower than those in radiation group (t=3.651, 5.293, 2.348 and 4.126, respectively, allP<0.05) , while slightly higher than those in control group. The levels of ICAM-1mRNA and NF-κB p65mRNA were significantly higher in radiation group than that in PDTC treatment group (allP<0.05) , There were no significant differences in these indicators between control group and PDTC group (P>0.05) .@*Conclusion@#The expression of ICAM-1mRNA and NF-κB p65mRNA is increased in rats with radiation-induced lung injury. Suggest that ICAM-1 and NF-κB are a key factor lead to radiation-induced lung injury. PDTC may inhibits NF-κB activity and further significantly deceases expression of ICAM-1, leading to significantly attenuated pulmonary inflammation and fibrosis, which provides a new therapeutic target for the prevention and treatment of radiation-induced lung injury.