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Carbon monoxide (CO), a metabolite of heme catalysis by heme oxygenase (HO), has been proposed to have anti-oxidative,anti-inflammatory and anti-apoptotic functions. Lipopolysaccharide (LPS)-induced lung injury (LI) is characterized by oxidativestress, inflammatory reaction and excessive pulmonary cell apoptosis. So we supposed that CO might have protection against LI. LIin rats was induced by intravenous injection of LPS (5 mg/kg). To observe the effect of CO inhalation, LI rats were exposed to 2.5×10-4(V/V) CO for 3 h. CO-induced changes of lung oxidative stress parameters, inflammatory cytokines, cell apoptosis, HO-1 expressionand histology were examined. Results revealed that expressions of the tumor necrosis factor-α (TNF-α) and interlukin-6 (IL-6),activities of maleic dialdehyde (MDA) and myeloperoxidase (MPO), and cell apoptosis in LPS injection + CO inhalation group were(0.91±0.25) pg/mg protein, (0.64±0.05) pg/mg protein, (1.02±0.23) nmol/mg protein, (7.18±1.62) U/mg protein and (1.60±0.34)%,respectively, significantly lower than the corresponding values in LI group [(1.48±0.23) pg/mg protein, (1.16±0.26) pg/mg protein,(1.27±0.33) nmol/mg protein, (8.16±1.49 ) U/mg protein and (3.18±0.51) %, P<0.05]. Moreover, CO inhalation obviously increasedthe expressions of HO-1 and interlukin-10 (IL-10) and activity of superoxide dismutase (SOD) [(5.43±0.92), (0.26±0.07) pg/mgprotein and (60.09±10.21) U/mg protein in LPS injection + CO inhalation group vs (3.08±0.82), (0.15±0.03) pg/mg protein and (50.98±6.88) U/mg protein in LI group, P<0.05]. LI was attenuated by CO inhalation. Our study demonstrates that inhalation of lowconcentration of CO protects lung against LPS-induced injury via anti-oxidant, anti-inflammation, anti-apoptosis and up-regulation ofHO-1 expression.