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首页> 外文期刊>The journals of gerontology.Series A. Biological sciences and medical sciences >Aging exacerbates microvascular endothelial damage induced by circulating factors present in the serum of septic patients.
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Aging exacerbates microvascular endothelial damage induced by circulating factors present in the serum of septic patients.

机译：老化加剧了败血症患者血清中存在的循环因子引起的微血管内皮损伤。

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The elderly patients show a significantly elevated mortality rate during sepsis than younger patients, due to their higher propensity to microvascular dysfunction and consequential multiorgan failure. We tested whether aging renders vascular endothelial cells more susceptible to damage induced by inflammatory factors present in the circulation during sepsis. Primary microvascular endothelial cells derived from young (3 months) and aged (24 months) Fischer 344 × Brown Norway rats were treated with sera obtained from sepsis patients and healthy controls. Oxidative stress (MitoSox fluorescence), death receptor activation (caspase 8 activity), and apoptotic cell death (caspase 3 activity) induced by treatment with septic sera were exacerbated in aged endothelial cells as compared with responses obtained in young cells. Induction of heme oxygenase-1 and thrombomodulin in response to treatment with septic sera was impaired in aged endothelial cells. Treatment with septic sera elicited greater increases in tumor necrosis factor-α expression in aged endothelial cells, as compared with young cells, whereas induction of inducible nitric oxide synthase, intercellular adhesion molecule-1, and vascular cell adhesion molecule did not differ between the two groups. Collectively, aging increases sensitivity of microvascular endothelial cells (MVECs) to oxidative stress and cellular damage induced by inflammatory factors present in the circulation during septicemia. We hypothesize that these responses may contribute to the increased vulnerability of elderly patients to multiorgan failure associated with sepsis.
机译：老年患者由于患有微血管功能障碍和随之而来的多器官功能衰竭的倾向较高，因此败血症期间的死亡率显着高于年轻患者。我们测试了老化是否使败血症期间循环中存在的炎性因子引起的血管内皮细胞更易受到损害。用从脓毒症患者和健康对照组获得的血清处理来自年轻（3个月）和年龄大（24个月）Fischer 344×Brown Norway大鼠的原代微血管内皮细胞。与在年轻细胞中获得的应答相比，在老化的内皮细胞中，由化脓性血清处理引起的氧化应激（MitoSox荧光），死亡受体激活（胱天蛋白酶8活性）和凋亡性细胞死亡（胱天蛋白酶3活性）加剧。在老化的内皮细胞中，对败血血清的治疗引起的血红素加氧酶-1和血栓调节蛋白的诱导作用减弱。与年轻细胞相比，化脓性血清治疗引起老年内皮细胞中肿瘤坏死因子-α表达的增加更大，而诱导型一氧化氮合酶，细胞间粘附分子-1和血管细胞粘附分子的诱导在两者之间没有区别组。总的来说，衰老增加了微血管内皮细胞（MVEC）对败血症期间循环中存在的炎症因子引起的氧化应激和细胞损伤的敏感性。我们假设这些反应可能导致老年患者对败血症引起的多器官衰竭的脆弱性增加。

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