Objective To observe the protection of carbon monoxide （CO） inhalation on lipopolysaccharide （LPS）-induced rat multiple organ injury. Methods Sprague-Dawley rats with multiple organ injury induced by 5 mg/kg LPS i...Objective To observe the protection of carbon monoxide （CO） inhalation on lipopolysaccharide （LPS）-induced rat multiple organ injury. Methods Sprague-Dawley rats with multiple organ injury induced by 5 mg/kg LPS intravenous injection were exposed to room air or 2.5 × 10 ^-4 （V/V） CO for 3 hours. The lung and intestine tissues of rats were harvested to measure the expression of heme oxygenase-1 （ HO-1 ） with reverse transcription-polymerase chain reaction, the levels of pulmonary tumor necrosis factor-or （ TNF-α）, interleukin-6 （ IL-6）, and intestinal platelet activator factor （ PAF）, intercellular adhesion molecule-1 （ICAM-1） with enzyme-linked immunosorbent assay, the content of maleic dialdehyde （MDA） and the activity of myeloperoxidase （MPO） with chemical method, the cell apoptosis rate with flow cytometry, and the pathological changes with light microscope. Results CO inhalation obviously up-regulated the expression of HO-1 in lung （5.43 ± 0. 92） and intestine （6. 29 ± 1.56） in LPS ＋ CO group compared with （ 3.08 ± 0. 82） and （ 3.97 ± 1.16 ） in LPS group （ both P 〈 0. 05 ）. The levels of TNF-ot, IL-6 in lung and PAF, ICAM-1 in intestine ofLPS ＋ CO group were 0. 91 ±0. 25,0. 64 ±0.05, 1. 19 ± 0. 52, and 1.83 ±0. 35 pg/mg, respectively, significantly lower than the corresponding values in LPS group （ 1.48 ± 0. 23, 1.16 ± 0. 26, 1.84 ± 0. 73, and 3.48 ± 0. 36 pg/mg, all P 〈 0. 05 ）. The levels of MDA, MPO, and cell apoptosis rate in lung and intestine of LPS ＋ CO group were 1.02 ± 0. 23 nmol/mg, 1.74 ± 0. 17 nmol/mg, 7.18 ± 1.62 U/mg, 6. 30 ±0. 97 U/mg, 1.60% ±0. 34%, and 30. 56% ±6. 33%, respectively, significantly lower than the corresponding values in LPS group （ 1.27 ± 0. 33 nmol/mg, 2. 75 ± 0. 39 nmol/mg, 8. 16 ± 1.49 U/mg, 7. 72 ± 1.07 U/mg, 3.18% ±0. 51%, and 41.52% -＋3.36%, all P 〈0.05）. In addition, injury of lung and intestine induced by LPS was attenuated at presence of CO inhalation. Conclusion CO inhalation protects rat lung and intestine from LPS-induced injury via anti-oxidantion, anti-inflammation, anti-apoptosis, and up-regulation of HO-1 expression.展开更多
文摘Objective To observe the protection of carbon monoxide （CO） inhalation on lipopolysaccharide （LPS）-induced rat multiple organ injury. Methods Sprague-Dawley rats with multiple organ injury induced by 5 mg/kg LPS intravenous injection were exposed to room air or 2.5 × 10 ^-4 （V/V） CO for 3 hours. The lung and intestine tissues of rats were harvested to measure the expression of heme oxygenase-1 （ HO-1 ） with reverse transcription-polymerase chain reaction, the levels of pulmonary tumor necrosis factor-or （ TNF-α）, interleukin-6 （ IL-6）, and intestinal platelet activator factor （ PAF）, intercellular adhesion molecule-1 （ICAM-1） with enzyme-linked immunosorbent assay, the content of maleic dialdehyde （MDA） and the activity of myeloperoxidase （MPO） with chemical method, the cell apoptosis rate with flow cytometry, and the pathological changes with light microscope. Results CO inhalation obviously up-regulated the expression of HO-1 in lung （5.43 ± 0. 92） and intestine （6. 29 ± 1.56） in LPS ＋ CO group compared with （ 3.08 ± 0. 82） and （ 3.97 ± 1.16 ） in LPS group （ both P 〈 0. 05 ）. The levels of TNF-ot, IL-6 in lung and PAF, ICAM-1 in intestine ofLPS ＋ CO group were 0. 91 ±0. 25,0. 64 ±0.05, 1. 19 ± 0. 52, and 1.83 ±0. 35 pg/mg, respectively, significantly lower than the corresponding values in LPS group （ 1.48 ± 0. 23, 1.16 ± 0. 26, 1.84 ± 0. 73, and 3.48 ± 0. 36 pg/mg, all P 〈 0. 05 ）. The levels of MDA, MPO, and cell apoptosis rate in lung and intestine of LPS ＋ CO group were 1.02 ± 0. 23 nmol/mg, 1.74 ± 0. 17 nmol/mg, 7.18 ± 1.62 U/mg, 6. 30 ±0. 97 U/mg, 1.60% ±0. 34%, and 30. 56% ±6. 33%, respectively, significantly lower than the corresponding values in LPS group （ 1.27 ± 0. 33 nmol/mg, 2. 75 ± 0. 39 nmol/mg, 8. 16 ± 1.49 U/mg, 7. 72 ± 1.07 U/mg, 3.18% ±0. 51%, and 41.52% -＋3.36%, all P 〈0.05）. In addition, injury of lung and intestine induced by LPS was attenuated at presence of CO inhalation. Conclusion CO inhalation protects rat lung and intestine from LPS-induced injury via anti-oxidantion, anti-inflammation, anti-apoptosis, and up-regulation of HO-1 expression.
