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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。
Objective To investigate the effect of aging on the expression of MCP-1 and ICAM-1 in lung tissue of rats with lipopolysaccharide-induced acute lung injury and to explore the possible mechanism of the susceptibility to inflammatory stimuli in aged rats. Methods The young and old rats were randomly divided into control group and LPS group. Immunohistochemistry was used to detect the ED-1 positive cells infiltration in the lung tissue of rats. Western blot and Northern blot were used to detect the protein and gene expression of MCP-1 and ICAM-1 in lung tissue respectively. Results (1) There were almost no ED-1 positive cells in the lungs of young and old control rats. After LPS injection, ED-1 positive cells infiltrated in both young and aged LPS groups were significantly increased, and the number of ED- P <0.05). (2) The basic amount of MCP-1 and ICAM-1 in the lung tissue of the young and old control rats were significantly different between the old and the young group. The levels of MCP-1 and MCP-1 in the young and old rats after LPS injection The expression of ICAM-1 was significantly up-regulated compared with the control group, and the up-regulation in the aged rats was more obvious with significant difference (P <0.05). The increase of MCP-1 and ICAM-1 expression at the same age was used as the variable to do t-test. The increase of MCP-1 and ICAM-1 expression in aged rats was still significantly higher than that in young rats (P <0.05). Conclusion Aging can up-regulate the expressions of MCP-1 and ICAM-1 in lung tissue and enhance the expression of MCP-1 and ICAM-1 induced by lipopolysaccharide, and aggravate the inflammatory reaction in lung.