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Protective effects of dexamethasone on early acute lung injury induced by oleic acid in rats

机译:地塞米松对大鼠油酸致急性肺损伤的保护作用

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Objective: Whether alveolar edema could be cleared by alveolar epithelial is a key to the treatment and prognosis of ALI (acute lung injury). In this study, oleic acid(OA)-induced ALI model was established, the expression of α1 Nasup+/sup/Ksup+/sup-ATPase (NKA) and β1 Nasup+/sup/Ksup+/sup-ATPase were performed in vivo to investigate the mechanism of alveolar fluid clearance (AFC) in ALI and the effect of early low doses of dexamethasone on alveolar fluid clearance. Methods: In this study, Male rats were challenged by OA with or without dexamethasone (1 mg/kg, iv) post-treatment. Lung histopathology, blood gas, pulmonary vascular permeability, BALF IL-6, MPO and NKA activity of lung were examined. α1NKA and β1NKA mRNA and protein expression were detected. Results: The results indicated that compared with sham operated group, NKA activity, mRNA and protein expression of α1NKA and β1NKA were decreased in OA treated group, while wet/dry ratio, lung index, IL-6, and MPO activity were increased significantly. Pulmonary edema was obviously seen under light microscope. Those indexes were improved in dexamethasone treated group compared to OA treated group. Conclusion: The expression of NKA to decline for the lung injury is one important mechanism of pulmonary edema. Early low dose of dexamethasone treatment could suppress the expression of inflammatory mediators, improved lung epithelial-endothelial barrier permeability, increased the expressions of α1 NKA and β1 NKA mRNA, α1 NKA and β1 NKA protein level, stimulated NKA activity and decreased pulmonary edema. In conclusion, these observations suggest that early low dose of dexamethasone treatment has a protective effect on OA induced ALI.
机译:目的:肺泡上皮能否清除肺泡水肿是急性肺损伤(ALI)的治疗和预后的关键。本研究建立了油酸诱导的ALI模型,表达了α 1 Na + / K + -ATPase(NKA)和& #x003b2; 1 Na + / K + -ATPase在体内进行了研究,以探讨ALI中肺泡液清除(AFC)的机制以及早期低剂量服用ATP的影响。地塞米松对肺泡液的清除作用。方法:在这项研究中,雄性大鼠在治疗后接受或不接受地塞米松(1 mg / kg,静脉注射)的OA攻击。检查肺的组织病理学,血气,肺血管通透性,BALF IL-6,MPO和肺NKA活性。检测到α 1NKA和β 1NKA mRNA和蛋白质表达。结果:结果表明,与假手术组相比,OA组降低了NKA活性,α 1NKA和β 1NKA mRNA和蛋白表达,而干湿比,肺指数,IL-6 ,MPO活性显着增加。光学显微镜下可见肺水肿。与OA组相比,地塞米松组的这些指标有所改善。结论:肺损伤中NKA表达下降是肺水肿的重要机制之一。早期低剂量地塞米松治疗可以抑制炎症介质的表达,改善肺上皮-内皮屏障通透性,增加α 1 NKA和β 1 NKA mRNA,α 1 NKA和&# x003b2; 1 NKA蛋白水平升高,刺激NKA活性并减少肺水肿。总之,这些观察结果表明,早期低剂量地塞米松治疗对OA诱导的ALI具有保护作用。

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