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目的研究增龄对纤维蛋白诱导急性肺损伤大鼠肺组织单核巨噬细胞趋化因子-1 (MCP-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根据腹腔注射不同的药物随机分为4组:对照组、脂多糖组、氨甲环酸组、肝素组。应用免疫组化分析纤维蛋白沉积;应用Western blot和Northern blot方法分别检测肺组织MCP-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均无纤维蛋白沉积,老年大鼠脂多糖组、氨甲环酸组和肝素组均比青年大鼠相同干预组纤维蛋白沉积明显,差别均有统计学意义(18．5％±3．1％对12．3％±2．1％,32．5％±5．4％对24．1％±4．5％和20．8％±3．6％对12．6％±1．8％,均为P<0．05);(2)青年和老年对照组大鼠肺组织内几乎无MCP-1表达,老年大鼠脂多糖组、氨甲环酸组和肝素组的MCP-1表达均较青年大鼠相同干预组上调,差异有统计学意义(0．40±0．02对0．20±0．03,0．60±0．05对0．25±0．04和0．30±0．01对0．20±0．04,均为P<0．05);(3)经纤维蛋白沉积增加量校正后,老年氨甲环酸组大鼠肺组织MCP-1的表达量仍显著高于青年大鼠氨甲环酸组(P<0．05)。结论纤维蛋白可上调急性肺损伤肺组织MCP-1基因及蛋白质表达,促进肺组织炎症反应;增龄能够促进肺组织纤维蛋白沉积,增强其上调肺组织MCP-1表达的作用。
Objective To investigate the effects of aging on the expression of MCP-1 in lung tissue of rats with acute lung injury induced by fibrin, 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 four groups according to the intraperitoneal injection of different drugs: control group, lipopolysaccharide group, tranexamic acid group, heparin group. Immunohistochemistry was used to analyze fibrin deposition. MCP-1 protein and gene expression were detected by Western blot and Northern blot respectively. Results (1) There was no fibrin deposition in the lungs of the young and old control rats. The levels of fibrin in the LPS rats, tranexamic acid and heparin groups were significantly higher than those in the young rats Statistically significant (18.5% ± 3.1% versus 12.3% ± 2.1%, 32.5% ± 5.4% vs. 24.1% ± 4.5%, and 20.8% ± 3.6% vs 12.6% ± 1.8%, both P <0.05); (2) There were almost no MCP-1 expression in the lungs of the young and old control rats, , Tranexamic acid group and heparin group MCP-1 expression were higher than the same intervention group of young rats, the difference was statistically significant (0.40 ± 0.02 vs 0.20 ± 0.03,0.60 ± 0.05 vs 0.25 ± 0.04 and 0.30 ± 0.01 vs. 0.20 ± 0.04, all P <0.05); (3) After adjustment for the increase in fibrin deposition, The expression of MCP-1 in trabetrocyte of tranexamic acid group was still significantly higher than that of tranexamic acid group (P <0.05). Conclusion Fibrin can up-regulate the expression of MCP-1 gene and protein in lung tissue of acute lung injury and promote the inflammatory reaction of lung tissue. Aging can promote the deposition of fibrin and enhance the expression of MCP-1 in lung tissue.