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目的:急性肺损伤是临床上常见的危重病,发病急,死亡率高,目前仍缺乏有效的治疗手段,新型的外源性硫化氢供体GYY4137具有抗炎、抗休克、抗癌及抗血栓等作用,本研究探讨其对脂多糖诱导的小鼠急性肺损伤的保护作用及其机制。方法:将BALB/c小鼠(18-20 g)随机分为3组:正常对照组(20只),脂多糖组(20只),治疗组(20只),然后复制小鼠脂多糖诱导的急性肺损伤模型:给予小鼠腹腔注射脂多糖(10 mg/kg)复制小鼠急性肺损伤模型模型,治疗组注射脂多糖1小时后给予腹腔注射GYY4137(50 mg/kg),在给予脂多糖8小时后将小鼠处死,留取血清与组织标本。检测小鼠血清中的炎症因子肿瘤坏死因子α、白介素6及白介素10的表达,检测小鼠血清中H2S的含量,测得肺脏湿/干比,检测肺组织中的髓过氧化物酶活性,并测得肺组织中与氧化应激相关的H2O2、·OH与SOD因子的含量。结果:脂多糖引起了严重的肺损伤,GYY4137对脂多糖导致的肺水肿、炎症反应及氧化应激损伤有不同程度的改善,保护了脂多糖造成的肺损伤,降低了脂多糖诱导的小鼠肺脏氧化应激损伤。其保护作用于抗炎、抗氧化有关。结论:GYY4137可能通过抗炎、抗氧化作用途径保护了脂多糖造成的急性肺损伤,可能在炎症疾病模型中也发挥相同作用,并且为未来临床使用缓释硫化氢供体提供了基础资料。
Objective: Acute lung injury is a common clinical critically ill disease, the incidence of acute and high mortality, there is still a lack of effective treatment, the new exogenous hydrogen sulfide donor GYY4137 with anti-inflammatory, anti-shock, anti-cancer and anti-thrombosis And other effects, the study to explore its lipopolysaccharide-induced acute lung injury in mice and its protective mechanism. Methods: BALB / c mice (18-20 g) were randomly divided into three groups: normal control group (20), lipopolysaccharide group (20), and treatment group (20) The model of acute lung injury was induced by intraperitoneal injection of lipopolysaccharide (10 mg / kg) in mice. One hour after the injection of lipopolysaccharide in the treatment group, intraperitoneal injection of GYY4137 (50 mg / kg) After 8 hours, the mice were killed and the serum and tissue samples were collected. Tumor necrosis factor-α, interleukin-6 and interleukin-10 were detected in the sera of mice. The content of H2S in the serum of the mice was measured. The lung wet / dry ratio was measured. The activity of myeloperoxidase in lung tissue was detected, The contents of H2O2, · OH and SOD in lung tissue were also measured. Results: Lipopolysaccharide caused severe lung injury. GYY4137 improved pulmonary edema, inflammation and oxidative stress injury induced by lipopolysaccharide, protected lung injury induced by lipopolysaccharide and decreased lipopolysaccharide induced mice Lung oxidative stress injury. Its protective effect on anti-inflammatory, anti-oxidation related. CONCLUSION: GYY4137 protects against acute lung injury induced by lipopolysaccharide through anti-inflammatory and anti-oxidant pathways. It may play the same role in inflammatory disease models and provides the basic information for future clinical use of sustained-release hydrogen sulfide donors.