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Release of exogenous carbon monoxide molecules on the inflammatory response in septic mice inhibited lung.doc

Release of exogenous carbon monoxide molecules on the inflammatory response in septic mice inhibited lung.doc

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Release of exogenous carbon monoxide molecules on the inflammatory response in septic mice inhibited lung

 PAGE \* MERGEFORMAT 17 Release of exogenous carbon monoxide molecules on the inflammatory response in septic mice inhibited lung Of: Zhang Ping, Zou forward, Stone G Health, Sun Bingwei [Abstract] Objective: To study the release of exogenous carbon monoxide molecules (carbon monoxide releasing molecules 2, CORM 2) intervention in septic mice inhibited lung inflammation. Methods: 18 male mice were randomly divided into sham operation group, CLP model group and CORM 2 intervention groups. production standard cecal ligation and puncture (cecal ligation and puncture, CLP) model of intervention with CORM 2 was observed in mice before and after intervention changes in lung inflammation. respectively, after CLP 6 h, 12 h, 24 h to collect plasma, lung tissue, enzyme-linked immunosorbent assay (ELISA), plasma tumor necrosis factor @ (TNF @) and interleukin 1 (IL 1) expression of inflammatory factors; detection of lung Tissue myeloperoxidase (MPO) activity, observed the extent of neutrophil aggregation; determination of lung wet dry weight ratio (W / D); hematoxylin eosin (HE) staining of lung tissue pathology; immune staining observed intercellular adhesion molecule (ICAM 1), pulmonary surfactant protein A (SP A) expression. Results: Compared with sham operation group, CLP model group, mainly for increased lung microvascular permeability, increased alveolar wall thickness, interstitial edema, leukocyte infiltration, MPO activity was significantly enhanced; inflammatory cytokines TNF @, IL 1 and IL 6 expression levels increased (P lt;0.05); with the CLP model group, CORM 2 intervention groups of interstitial lung edema reduced leukocyte infiltration significantly reduced the expression of these inflammatory cytokines significantly inhibited (P lt;0.05). Conclusion: CDRM 2 significantly inhibited the inflammatory cytokines in sepsis and ICAM 1, SP A expression, decreased MPO activity, the decrease accumulation of neutrophils, reduce tissue inflammation, and lung in

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