tailieunhanh - Báo cáo y học: " Low-molecular-weight heparin reduces hyperoxiaaugmented ventilator-induced lung injury via serine/threonine kinase-protein kinase B"

Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học 'Respiratory Research cung cấp cho các bạn kiến thức về ngành y đề tài:" Low-molecular-weight heparin reduces hyperoxiaaugmented ventilator-induced lung injury via serine/threonine kinase-protein kinase B. | Li et al. Respiratory Research 2011 12 90 http content 12 1 90 RESPIRATORY RESEARCH RESEARCH Open Access Low-molecular-weight heparin reduces hyperoxia-augmented ventilator-induced lung injury via serine threonine kinase-protein kinase B Li-Fu Li1 2 3 Cheng-Ta Yang1 2 3 Chung-Chi Huang1 2 3 Yung-Yang Liu4 5 Kuo-Chin Kao1 2 3 and Horng-Chyuan Lin1 2 3 Abstract Background High-tidal-volume mechanical ventilation and hyperoxia used in patients with acute lung injury ALI can induce the release of cytokines including high-mobility group box-1 HMGB1 oxygen radicals neutrophil infiltration and the disruption of epithelial and endothelial barriers. Hyperoxia has been shown to increase ventilator-induced lung injury but the mechanisms regulating interaction between high tidal volume and hyperoxia are unclear. We hypothesized that subcutaneous injections of enoxaparin would decrease the effects of hyperoxia on high-tidal-volume ventilation-induced HMGB1 production and neutrophil infiltration via the serine threonine kinase protein kinase B Akt pathway. Methods Male C57BL 6 either wild type or Akt - aged between 6 and 8 weeks weighing between 20 and 25 g were exposed to high-tidal-volume 30 ml kg mechanical ventilation with room air or hyperoxia for 2 to 8 hours with or without 4 mg kg enoxaparin administration. Nonventilated mice served as a control group. Evan blue dye lung wet-to-dry weight ratio free radicals myeloperoxidase Western blot of Akt and gene expression of HMGB1 were measured. The expression of HMGB1 was studied by immunohistochemistry. Results High-tidal-volume ventilation using hyperoxia induced microvascular permeability Akt activation HMGB1 mRNA expression neutrophil infiltration oxygen radicals HMGB1 production and positive staining of Akt in bronchial epithelium. Hyperoxia-induced augmentation of ventilator-induced lung injury was attenuated with Akt deficient mice and pharmacological inhibition of Akt activity by enoxaparin. .