NF-κB信号通路在低分子量多环芳烃致肺部炎症中的作用机制研究OA

Objective To investigate the mechanism by which low molecular weight polycyclic aromatic hydrocarbons(LMW-PAHs)induce pulmonary inflammatory injury through the activation of the nuclear fac-tor kappa-B(NF-κB)/phosphorylation nuclear factor κB(p-NF-κB)signaling pathway via oxidative stress.Methods An LMW-PAHs-exposed animal model was established.Pathological changes in rat lung tissue were observed.Protein expression levels of pulmonary inflammatory mediators interleukin-1β(IL-1β)and IL-4 were detected.The oxidative stress markers glutathione peroxidase(GSH-PX)and total antioxidant capacity(T-AOC),and the expression levels of NF-κ B signaling pathway proteins were observed to investigate the mechanisms by which LMW-PAHs induce pulmonary inflammation.Results Compared with the control group,all exposed groups showed decreased T-AOC concentration and GSH-PX activity(P<0.05);NF-κB/p-NF-κB protein activity was significantly elevated(P<0.05);IL-1β levels were significantly increased in the high-dose group(P<0.05);IL-4 levels were significantly reduced across all dose groups(P<0.05).Conclusion LMW-PAHs induce oxidative stress,thereby activating the NF-κB signaling pathway to promote inflammatory cytokine release,thus resulting in inflammatory lung injury.