CAJ | 학술논문

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.
목적 연구증령대지다당유도급성폐손상대서폐조직MCP-1화ICAM-1표체적영향,탐토노년대서대염성자격역감적가능궤제.방법 청년급노년대서균수궤분위대조조화LPS조.응용면역조화기술검측대서폐조직ED-1양성세포침윤정황,응용Western blot화Northern blot분별검측폐조직MCP-1화ICAM-1단백질화기인표체.결과 (1)청년화노년대조조대서폐조직내궤호무ED-1양성세포,주사LPS후,청년화노년LPS조ED-1양성세포침윤균명현증강,병차노년서명현다우청년서(P<0.05).(2)청년화노년대조조대서폐조직내균유기출량적MCP-1화ICAM-1표체,노년여청년조지간유현저성차이,주사LPS후청년화노년대서MCP-1화ICAM-1표체균교대조조현저상조,노년대서상조경가명현,구유현저성차이(P<0.05).이상동서령MCP-1화ICAM-1표체적증가량위변량,진행t검험,발현노년MCP-1화ICAM-1표체적증가량잉현저고우청년대서(P<0.05).결론 증령가상조폐조직MCP-1、ICAM-1표체,병가강지다당유도MCP-1、ICAM-1표체적작용,가중폐부염증반응.
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. Immanohistochemistry for of ED-1 was used to detect the infilwating 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 (P<0.05), and the increment was more obviously in the aged group (P<0.05). In the two normal control groups, the aged rats showed significantly higher expressions of MCP-1 and ICAM-1 than the young rats (P<0.05); LPS significantly up-regulated their expression in the young and aged groups (P<0.05), but the latter showed greater increments (P<0.05). The aged rats with ALI also showed significantly greater MCP-1 and ICAM-1 increments than those of the young rats (P<0.05). 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.