摘要
目的 探讨地塞米松 (Dex)对创伤性急性肺损伤 (ALI)治疗作用的可能机制。方法 采用逆转录聚合酶链反应 (RT PCR)、酶联免疫吸附法 (ELISA)检测 2 4只大耳白兔肺组织肿瘤坏死因子 α基因 (TNF αmRNA)表达及肺泡巨噬细胞 (AM )培养上清液中肿瘤坏死因子 α (TNF α)、白细胞介素 (IL) 6水平。结果 创伤性ALI兔肺组织TNF αmRNA表达及AM培养上清液中TNF α ,IL 6含量较正常对照组比较明显升高 (P <0 .0 1)。Dex治疗后能显著下调TNF αmRNA的表达 (6 8% ,P <0 .0 1) ,降低AM分泌TNF α(P <0 .0 5 )及IL 6水平 (P <0 .0 1)。结论 Dex能缓解创伤性ALI的发生、发展。其机制与其对TNF α、IL
Objective To explore the possible mechanism of dexamethasone (Dex) in the treatment of traumatic acute lung injury (ALI).Methods Reverse transcription ploymerase chain reaction (RT PCR) and enzyme linked immune adsorbing analysis (ELISA) methods were used to detect the TNF α mRNA expression in lung tissues and TNF α, IL 6 levels of the supernatant from the cultured alveolar macrophages (AM) in 24 rabbits. Results As compared with normal control group, the levels of TNF α and IL 6 released by AM and TNF α mRNA expression in lung tissues were significantly increased in the rabbits with traumatic ALI ( P < 0.01 ).Dex could effectively inhibit the expression of pulmonary TNF α mRNA (68 %, P <0.01) and reduce TNF α ( P <0.05) and IL 6 ( P <0.01) levels released by AM in traumatic ALI rabbits. Conclusion Dex could prevent the development and progression of traumatic ALI, which was contributed to the regulatory roles of Dex on pro inflammatory factors,such as TNF α and IL 6. [
出处
《中华实验外科杂志》
CAS
CSCD
北大核心
2001年第1期60-61,共2页
Chinese Journal of Experimental Surgery
基金
国家自然科学基金资助项目 !(39770 736)
关键词
地塞米松
急性肺损伤
肿瘤坏死因子-Α
基因表达
Dexamethasone
Trauma
Acute lung injury
Tumor necrosis factor α
Gene expression
