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Preserved Immune Functions and Controlled Leukocyte Oxidative Stress in Naturally Long-lived Mice: Possible Role of Nuclear Factor Kappa B

机译:自然长寿小鼠中的免疫功能和白细胞氧化应激的控制:核因子κB的可能作用

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摘要

In order to verify the survival biomarker role of several immune functions, and to determine the oxidation and inflammation mechanisms underlying variability in the aging process, we have investigated a variety of immune functions and oxidative stress parameters as well as activation of the nuclear factor kappa B (NFkB) in peritoneal leukocytes from four different age groups of mice, including natural extreme longevity. Immune cells from naturally long-lived animals showed preservation of immune function in response to stimuli and controlled oxidative stress as well as nuclear factor kappa B activation in resting conditions. Moreover, leukocytes from extreme long-lived animals showed increased catalase activity when compared with the adults. In contrast, the old and very old animal groups showed impaired immune function and increased oxidation as well as NFkB activation. Our results support preserved immune function as a biomarker of extended survival and point to controlled regulation of NFkB activity as a key mechanism restraining oxidative stress in immune cells and contributing to reach longevity.
机译:为了验证几种免疫功能的生存生物标志物作用,并确定衰老过程中变异性的氧化和炎症机制,我们研究了多种免疫功能和氧化应激参数以及核因子κB的活化(NFkB)来自四个不同年龄组的小鼠腹膜白细胞,包括自然的长寿。来自自然长寿动物的免疫细胞在休息条件下对刺激和受控的氧化应激以及核因子κB的活化具有免疫功能的保持。此外,与成年动物相比,极端长寿动物的白细胞显示出过氧化氢酶活性增加。相比之下,成年和非常老的动物群均显示出免疫功能受损,氧化增加以及NFkB活化。我们的结果支持保留的免疫功能,作为延长生存时间的生物标志物,并指出对NFkB活性的受控调节是抑制免疫细胞中氧化应激并有助于延长寿命的关键机制。

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