Objective    To investigate the role of NF-κB in acute lung injury following intracerebral hemorrhage.     Methods    Using stereotactic apparatus we infused autologous blood into the caudate nucleus to build up rat  ICH model. A total of 35 male adult Wistar rats were randomly divided into sham-operation group(n=5) and hemorrhage group(n=30) that was subsequently divided into 6 subgroups (6 h

12 h

24 h

48 h

3 d

and 5 d

n=5). The inflammatory reaction degrees in the peripheral tissues of hematoma in the brain and lung were observed after HE staining. The levels of NF-κB p65 mRNA in the brain and lung were assayed using RT-PCR. The content of TNF-α and IL-1β in serum was determined by radioimmunoassay (RIA) method.     Results    Brain edema was obvious at 12 h after intracerebral hemorrhage and the inflammatory cells infiltration increased at 24 h and reached maximum at 48 h in the peripheral tissues of hematoma. Interstitial pneumonia and local emphysema appeared at 6 h and got to peak at 48-72 h

in which alveolar structure was significantly destroyed. In comparison with sham-operation group

the expression of NF-κB p65 mRNA began to increase at 6 h in brain and lung tissues (P0.01)

and reached maximum at 48 h (P0.01). Thereafter it began decreasing but was still higher at 5 d (P0.01). The content of serum TNF-α began to increase at 6 h

got to peak at 48 h

and still higher than the sham-operation group at 5 d (P0.01). The content of IL-1β did not increase among all intracerebral hemorrhage groups.     Conclusion    Intracerebral hemorrhage can induce acute lung injury through irritating the cascade of inflammation. NF-κB plays a critical role in the pathophysiology of inflammation.