Up-regulation of heme oxygenase-1 by sevoflurane attenuates LPS-induced acute lung injury in a rat model
Zhao Shuangping
Abstract
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Zhao Shuangping
Abstract
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To investigate heme oxygenase-1(HO-1) expression induced by sevoflurane in lipopolysaccharide (LPS)-induced acute lung injury (ALI). Forty-eight rats were randomly designated into six groups to receive normal saline (NS), ZnPPIX(a specific HO-1 inhibitor), or sevoflurane: A (control, NS only), B (ZnPPIX only), C (sevoflurane only), D (LPS + 1.0 minimum alveolar concentration (MAC) sevoflurane), E (ZnPPIX + LPS +1.0 MAC sevoflurane) and F (LPS only). We evaluated the histopathologic changes, W/D ratio, and the activity of SOD, MDA, MPO, and HO-1 using the traditional methods. The mRNA and protein expression of ICAM-1, CINC, and HO-1 was detected by RT-PCR and western blotting. No significant difference was observed between group A, B, and C. LPS treatment (group D, E and F) could elicit serious lung injury in histopathology. The wet/dry ratio, MDA, MPO, and HO-1 activity, the mRNA and protein expression of ICAM-1 and CINC were significantly increased after LPS treatment (p < 0.05). Sevoflurane post-conditioning (Group F) could further promote HO-1 up-regulated expression and effectively protect ALI with decreasing pathomorphological scores, MPO activity, W/D, and the mRNA and protein expression of ICAM-1, and CINC. Sevoflurane post-conditioning may be an effective inducer to up-regulate HO-1 expression to alleviate ALI. Key words: Sevoflurane, acute lung injury, HO-1.
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To investigate heme oxygenase-1(HO-1) expression induced by sevoflurane in lipopolysaccharide (LPS)-induced acute lung injury (ALI). Forty-eight rats were randomly designated into six groups to receive normal saline (NS), ZnPPIX(a specific HO-1 inhibitor), or sevoflurane: A (control, NS only), B (ZnPPIX only), C (sevoflurane only), D (LPS + 1.0 minimum alveolar concentration (MAC) sevoflurane), E (ZnPPIX + LPS +1.0 MAC sevoflurane) and F (LPS only). We evaluated the histopathologic changes, W/D ratio, and the activity of SOD, MDA, MPO, and HO-1 using the traditional methods. The mRNA and protein expression of ICAM-1, CINC, and HO-1 was detected by RT-PCR and western blotting. No significant difference was observed between group A, B, and C. LPS treatment (group D, E and F) could elicit serious lung injury in histopathology. The wet/dry ratio, MDA, MPO, and HO-1 activity, the mRNA and protein expression of ICAM-1 and CINC were significantly increased after LPS treatment (p < 0.05). Sevoflurane post-conditioning (Group F) could further promote HO-1 up-regulated expression and effectively protect ALI with decreasing pathomorphological scores, MPO activity, W/D, and the mRNA and protein expression of ICAM-1, and CINC. Sevoflurane post-conditioning may be an effective inducer to up-regulate HO-1 expression to alleviate ALI. Key words: Sevoflurane, acute lung injury, HO-1.
Key concepts: Sevoflurane, Heme oxygenase, Lipopolysaccharide, Chemistry, Pharmacology, Lung, Messenger RNA, Heme