论文部分内容阅读
目的:探讨联合应用乌司他丁和甲基泼尼松龙对内毒素(lipopolysaccharide,LPS)所致急性肺损伤(acute lung injury,ALI)大鼠的保护作用及机制。方法:舌下静脉注射LPS(5 mg.kg-1)建立大鼠急性肺损伤模型;将120只Wistar大鼠,随机分成5组:正常对照组(10 mL.kg-1)、模型对照组(10 mL.kg-1)、甲基泼尼松龙组(20 mg.kg-1)、乌司他丁组(10万U.kg-1)、联合治疗组即甲基泼尼松龙+乌司他丁组(15 mg.kg-1+10万U.kg-1),给药后于2,6,12,24 h分批处死大鼠;采用ELISA法检测血清IL-6和TNF-a水平,同时应用ELISA法观察肺组织NF-κB/p65相对含量和逆转录PCR检测肺组织TNF-аmRNA表达情况;并进行统计学分析。结果:与正常对照组比较,模型对照组及用药各组血清IL-6,TNF-a,肺组织NF-κB/p65和TNF-аmRNA均明显升高,差异有统计学意义(P<0.05);甲基泼尼松龙组、乌司他丁组、联合治疗组与模型对照组比较,差异有统计学意义(P<0.05);联合治疗组与甲基泼尼松龙组、乌司他丁组比较,差异有统计学意义(P<0.05)。结论:联合应用乌司他丁和甲基泼尼松龙可降低内毒素(LPS)所致ALI大鼠血清IL-6,TNF-a升高,并显著抑制肺组织NF-κB/p65蛋白和TNF-аmRNA表达。
Objective: To investigate the protective effect and mechanism of ulinastatin and methylprednisolone on acute lung injury (ALI) induced by lipopolysaccharide (LPS) in rats. Methods: Acute lung injury model was established by sublingual intravenous injection of LPS (5 mg.kg-1). 120 Wistar rats were randomly divided into 5 groups: normal control group (10 mL.kg-1), model control group (10 mL.kg-1), methylprednisolone group (20 mg.kg-1) and ulinastatin group (100 000 U.kg-1). The combination therapy group was methylprednisolone + Ulinastatin group (15 mg.kg-1 + 100 000 U.kg-1). Rats were sacrificed at 2, 6, 12 and 24 h after administration. The levels of IL-6 and IL- At the same time, the relative content of NF-κB / p65 in lung tissue and the expression of TNF-а mRNA in lung tissue were detected by reverse transcription polymerase chain reaction (ELISA). Results: Compared with the normal control group, the levels of IL-6, TNF-a, NF-κB / p65 and TNF-аmRNA in the model control group and the treated groups were significantly increased ; Methylprednisolone group, ulinastatin group, combined treatment group and the model control group, the difference was statistically significant (P <0.05); combination therapy group and methylprednisolone group, ulinastat The difference was statistically significant (P <0.05). Conclusion: Combination of ulinastatin and methylprednisolone can reduce the serum levels of IL-6 and TNF-α in ALI rats induced by endotoxin (LPS), and significantly inhibit the expression of NF-κB / p65 protein and TNF-а mRNA expression.