HCA treatment significantly enhanced HO-1 protein expression and activity in IR-induced lung injury; (2) HCA attenuated IR-induced lung injury as evidenced by decreased pulmonary edema, reduced PAP, inhibition of the inflammatory response, attenuated apoptosis, improved lung pathology, and suppressed IKK-β phosphorylation, IκB-α degradation, and nuclear translocation of NF-κB, and (3) the protection provided by HCA can be damped by the HO-1 activity inhibitor, ZnPP. This evidence concerns the gene NFKB1 and edema.