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目的 :研究抑制一氧化氮对脂多糖 (LPS)诱导肺损伤炎症反应的影响。方法 :ELISA检测TNFα、IL 1β、IL 6和IL 10浓度 ,Griess法测定亚硝酸盐浓度。肺湿干重比反映小鼠肺损伤程度。结果 :小鼠腹腔注射LPS 2 0mg/kg后 ,血浆及肺泡灌洗液 (BALF)中TNFα、IL 1β、IL 6、IL 10和亚硝酸盐浓度显著升高。LPS注射前 30min给予地塞米松 70mg/kg,血浆TNFα、IL 1β、IL 6、IL 10及亚硝酸盐浓度明显降低 ,而BALF中IL 1β、IL 6、IL 10浓度明显降低。给予一氧化氮合酶抑制剂S 硫酸甲基异硫脲 (SMT) 85mg/kg ,血浆IL 1β和IL 6明显升高 ,BALF中TNFα明显升高 ,而IL 1β、IL 6和IL 10无明显改变。与LPS组相比 ,地塞米松组肺湿干重比明显降低 ,而SMT组相反。结论 :抑制一氧化氮引起促炎性细胞因子释放增加 ,并加重肺损伤。
AIM: To investigate the effects of nitric oxide on the inflammatory response induced by lipopolysaccharide (LPS) in lung injury. Methods: The concentrations of TNFα, IL 1β, IL 6 and IL 10 were detected by ELISA. The nitrite concentration was determined by Griess method. Lung wet weight ratio reflects the degree of lung injury in mice. Results: After intraperitoneal injection of LPS 20 mg / kg, the concentrations of TNFα, IL 1β, IL 6, IL 10 and nitrite in BALF were significantly increased. LPS injection of dexamethasone 70mg / kg 30min before injection, plasma TNFα, IL 1β, IL 6, IL 10 and nitrite concentrations were significantly reduced, while IL 1β, IL 6, IL 10 concentrations were significantly reduced. Administration of 85 mg / kg of nitric oxide synthase inhibitor, methyl thiosulfate (SMT), significantly increased plasma levels of IL-1β and IL-6, significantly increased TNFα in BALF, and no significant changes in IL 1β, IL 6 and IL 10 change. Compared with the LPS group, the lung wet / dry weight ratio in dexamethasone group was significantly decreased, while the SMT group was the opposite. Conclusion: Inhibition of nitric oxide causes an increase in the release of proinflammatory cytokines and aggravates lung injury.