摘要
目的探讨基质金属蛋白酶(MMPs)和细胞外基质金属蛋白酶诱导因子(EMMPRIN)在高氧所致急性肺损伤(ALI)发病中的作用。方法72只小鼠按随机数字表法分为正常对照组和高氧24、48、72h组,每组18只。高氧组小鼠置于密闭的氧气室,暴露于体积分数>98%的高氧;正常对照组小鼠呼吸室内空气作为对照组。分别于24、48和72h活杀高氧组小鼠,取肺评价肺损伤程度;逆转录聚合酶链反应(RT PCR)及免疫组化法测定肺组织MMP2、MMP9及EMMPRIN的mRNA和蛋白表达及组织分布。结果高氧能引起ALI。RT PCR结果显示,高氧组动物肺组织MMP2、MMP9及EMMPRIN的mRNA表达均增高;免疫组化研究显示,MMP2和MMP9蛋白主要表达于气道上皮细胞、血管平滑肌细胞和炎性细胞的胞浆中,EMMPRIN蛋白则主要表达于上述细胞胞浆和细胞膜上;它们在气道上皮细胞中的表达在高氧环境下明显升高。结论高氧能引起ALI,伴MMP2、MMP9和EMMPRIN的表达增高,MMPs通过降解细胞外基质从而在高氧所致ALI过程中发挥重要作用。
Objective To investigate the role of matrix metalloproteinases （MMPs） and extracellular matrix metalloproteinase inducer （EMMPRIN） in the pathogenesis of acute lung injury induced by hyperoxia. Methods Fifty-four mice were exposed in sealed cages to 〉98% oxygen （for 24 - 72 hours）, and another 18 mice to room air. The severity of lung injury was assessed, and the expression of mRNA and protein of MMP - 2, MMP - 9 and EMMPRIN in lung tissue, after exposure for 24, 48 and 72 hours of hyperoxia were studied by reverse transcription- polymerase chain reaction （RT-PCR） and immunohistochemistry. Results Hyperoxia caused acute lung injury~ this was accompanied by increased expression of an upregulation of MMP - 2, MMP - 9 and EMMPRIN mRNA and protein in lung tissues. Conclusion Hyperoxia causes acute lung injury in mice;increases in MMP - 2, MMP - 9 and EMMPRIN may play an important role in the development of hyperoxia-induced lung injury in mice.
出处
《中国危重病急救医学》
CAS
CSCD
北大核心
2006年第8期449-451,F0005,共4页
Chinese Critical Care Medicine
基金
卫生部卫生局留学人员资助项目(2004局019)
关键词
高氧
肺损伤
急性
基质金属蛋白酶
hyperoxia
acute lung injury
matrix metalloproteinase
