目的探讨炎性衰老的炎性细胞因子网络机制,及淫羊藿总黄酮(epimedium total flavonoids,EF)干预的效果与机制。方法清洁级健康雄性SD大鼠分为3组:4月龄(4 m)组、24月龄(24 m)组和24月龄加EF干预(24 m+EF)组,每组10只。自满21月龄当天开始,24 m+EF组予EF灌胃,24 m组给予等量蒸馏水灌胃,均连续90 d。取各组大鼠海马组织,应用炎症细胞因子与受体基因芯片对海马组织分别进行基因表达检测,绘制基因表达谱,筛选有表达差异的基因。海马组织匀浆,离心取上清液,运用酶联免疫吸附法检测上清液中炎性细胞因子肿瘤坏死因子-α(TNF-α)、白介素-6(IL-6)和IL-10蛋白表达。结果在海马组织中,与4 m组相比,24 m组表达上调的促炎性反应细胞因子与受体基因有9个,表达下调的抗炎性细胞因子与受体基因有6个。与24 m组比较,24 m+EF组中表达上调的抗炎性细胞因子与受体基因有8个,表达下调的促炎性细胞因子与受体基因有11个。24 m组海马组织中TNF-α和IL-6水平都显著高于4 m组(P<0.01);与24 m组比较,24 m+EF组中TNF-α和IL-6水平都明显降低,IL-10水平显著升高(P<0.01)。与4 m组相比,24 m组海马组织上清液中TNF-α/IL-10和IL-6/IL-10比值均显著升高(P<0.01);24 m+EF组TNF-α/IL-10和IL-6/IL-10比值均比24 m组显著降低(P<0.01)。结论老年大鼠海马存在促炎性细胞因子表达上调,导致促-抗炎性细胞因子网络和促-抗炎反应体系平衡失调,这可能是炎性衰老中出现高促炎性反应状态的原因和炎性衰老发生的新机制;EF可能通过下调促炎性细胞因子表达和上调抗炎性细胞因子表达,重塑促-抗炎性细胞因子网络和促-抗炎性反应体系新的平衡,达到干预炎性衰老的目的。 Objective To explore the inflammatory cytokines network mechanism of inflammatory senescence and the effect and mechanism of epimedium total flavonoids (EF) intervention. Methods Healthy male Sprague-dawley rats were divided into 3 groups: 4-month-old (4 m), 24-month old (24 m) and 24-month-old plus EF intervention (24 m + EF). From the age of 21 months of complacency, 24 m + EF group was given intragastric administration of EF, while the 24 m group was administered with equal volume of distilled water for continuous 90 d. The hippocampus tissues of each group were taken, and the gene expression of hippocampus was detected by using inflammatory cytokines and receptor gene chips. The gene expression profiles were drawn and the genes with different expression were screened. The hippocampus was homogenized and the supernatant was centrifuged. The levels of inflammatory cytokines TNF-α, IL-6 and IL-10 in the supernatant were detected by enzyme linked immunosorbent assay expression. Results In the hippocampus, compared with the 4-m group, there were 9 proinflammatory cytokine and receptor genes that were up-regulated in the 24-m group and 6 anti-inflammatory cytokines and receptor genes were down-regulated in the hippocampus. Compared with 24 m group, there were 8 anti-inflammatory cytokines and receptor genes that were up-regulated in 24 m + EF group, while 11 genes were down-regulated. The levels of TNF-α and IL-6 in 24 m hippocampus were significantly higher than those in 4 m group (P <0.01). Compared with 24 m group, the levels of TNF-α and IL-6 in 24 m + EF group were significantly decreased , IL-10 levels were significantly increased (P <0.01). Compared with 4 m group, the ratios of TNF-α / IL-10 and IL-6 / IL-10 in 24 m hippocampal tissue supernatants were significantly increased (P <0.01) / IL-10 and IL-6 / IL-10 ratio were significantly lower than 24 m group (P <0.01). Conclusion The up-regulation of proinflammatory cytokines in the hippocampus of aged rats leads to imbalance of pro-anti-inflammatory cytokines network and pro-anti-inflammatory reaction system, which may be the reason of the high inflammatory reaction state in inflammatory senescence and New mechanism of inflammatory senescence; EF may be through the downregulation of proinflammatory cytokine expression and up-regulation of anti-inflammatory cytokine expression, remodeling pro-anti inflammatory cytokine network and pro-anti-inflammatory reaction system, a new balance of Interventional inflammatory aging purposes.