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增龄对急性肺损伤大鼠肺组织ICAM-1和MCP-1表达的影响

ISSN号：1673-4254
期刊名称：《南方医科大学学报》
时间：0
分类：R332[医药卫生—人体生理学;医药卫生—基础医学]
作者机构：[1]解放军总医院肾科/解放军肾病中心暨全军重点实验室,北京100853
相关基金：“973”国家重大基础研究发展规划基金; 国家自然科学基金创新研究群体基金（30121005）; 国家自然科学基金（30470803）

作者：林淑芃[1], 孙雪峰[1], 陈香关[1], 师锁柱[1], 洪权[1], 吕杨[1]

关键词：脂多糖, 急性肺损伤, 单核巨噬细胞趋化蛋白-1, 细胞间粘附分子-1, 大鼠, lipopolysaccharide, acute lung injury, monocyte chemoattractant protein-1, intercellular adhesion molecule 1, rats

中文摘要：

目的研究增龄对脂多糖诱导急性肺损伤大鼠肺组织MCP-1和ICAM-1表达的影响,探讨老年大鼠对炎性刺激易感的可能机制。方法青年及老年大鼠均随机分为对照组和LPS组。应用免疫组化技术检测大鼠肺组织ED-1阳性细胞浸润情况,应用Western blot和Northern blot分别检测肺组织MCP-1和ICAM-1蛋白质和基因表达。结果（1）青年和老年对照组大鼠肺组织内几乎无ED-1阳性细胞,注射LPS后,青年和老年LPS组ED-1阳性细胞浸润均明显增强,并且老年鼠明显多于青年鼠（P〈0.05）。（2）青年和老年对照组大鼠肺组织内均有基础量的MCP-1和ICAM-1表达,老年与青年组之间有显著性差异,注射LPS后青年和老年大鼠MCP-1和ICAM-1表达均较对照组显著上调,老年大鼠上调更加明显,具有显著性差异（P〈0.05）。以相同鼠龄MCP-1和ICAM-1表达的增加量为变量,进行t检验,发现老年MCP-1和ICAM-1表达的增加量仍显著高于青年大鼠（P〈0.05）。结论增龄可上调肺组织MCP-1、ICAM-1表达,并加强脂多糖诱导MCP-1、ICAM-1表达的作用,加重肺部炎症反应。

英文摘要：

Objective To investigate the effect of aging on the expressions of monocyte chemoattractant protein 1 （MCP-1） and intercellular adhesion molecule 1 （ICAM-1） in the lung tissue of rats with lipopolysaccharide （LPS）-induced acute lung injury （ALI）. Methods Both young （3 months old） and aged （27 months old） female Wistar rats were randomly divided into two groups （n=8）, namely the normal control and LPS-induced ALI groups. Immunohistochemistry for of ED-1 was used to detect the infiltrating inflammatory cells. Western blot and Northern blot analyses were employed for evaluating the expressions of MCP-1 and ICAM-1 at the protein and mRNA levels. Results Virtually no ED-1-positive cells were found in the lung tissue of the control rats in the young and aged groups. After LPS-induced ALI, ED-1-positive cells in the lung tissues increased significantly in both young and aged groups （P0.05）, and the increment was more obviously in the aged group （P0.05）. In the two normal control groups, the aged rats showed significantly higher expressions of MCP-1 and ICAM-1 than the young rats （P0.05）; LPS significantly up-regulated their expression in the young and aged groups （P0.05）, but the latter showed greater increments （P0.05）. The aged rats with ALI also showed significantly greater MCP-1 and ICAM-1 increments than those of the young rats （P0.05）. Conclusions Aging may upregulate lung MCP-1 and ICAM-1 expressions and enhance LPS-induced increments of MCP-1 and ICAM-1 expressions to exacerbate the pulmonary inflammation in rats.

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