1. Department of Respiratory Medicine, Clinical Medical College of Navy, Second Military Medical University, Beijing 100048, China; 2. Political Department Clinic of Shenyang Military Area Command, Shenyang 110032, China; 3. Pulmonary and Critical Care Medicine of PLA Navy General Hospital, Beijing 100048, China
Abstract:Objective To investigate the mechanisms of inhaled hydrogen sulfide inhibiting oxidative stress of cotton smoke inhalation-induced acute lung injury in rats. Methods Twenty-four male SD rats were randomly allocated into control group, H2S group, smoke group and smoke+H2S group. The rat model of cotton smoke inhalation injury was established. After smoke inhalation or simulated smoke inhalation, rats inhaled H2S 80 ppm, 30% oxygen for 6 hours (H2S group and smoke+H2S group), or rats inhaled 30% oxygen for 6 hours (control group and smoke group). Then rats were mercy killed. In each group of rats we observed the concentration of NO,iNOS,NF-κB p65,MDA in homogenized lung tissue by ELISA,used the method of fluorescence quantitative PCR to detect the expression of iNOS mRNA in homogenized lung tissue, and immunohistochemically detected the relative expression of NF-κB p65 with Image Pro Plus 6.0 software. Results Compared with the control group, concentrations of MDA, NO, iNOS, NF-κB p65, relative expression of iNOS mRNA and sum IOD of NF-κB p65 in the smoke group rats’ homogenized lung tissue were significantly elevated, and those in the smoke+H2S group were relatively lower, for example, concentrations of NF-κB p65 were (8123.51±2095.33) pg/ml vs (13803.19±2196.37) pg/ml, P<0.001; relative expression of iNOS mRNA was (1.04±0.24) vs (2.20±0.21), P<0.001. Concentrations of iNOS, relative expression of iNOS mRNA and sum IOD of NF-κB p65 in the H2S group were higher than those in the control group, meanwhile concentrations of MDA, NO, NF-κB p65 in the H2S group were similar to those in the control group. Conclusions The mechanisms of inhaled 80 ppm hydrogen sulfide for 6 hours protecting against cottn smoke inhalation-induced ALI in rats potentially is inhaled hydrogen sulfide inhibiting the activation of NF-κB p65, so the expression of iNOS mRNA, iNOS and NO grow downwards and as a result, it relieves oxidative stress and reduces pathological damage to lung tissue.