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炎症和氧化应激作为智力障碍患者早衰的生物标志物。

Inflammation and oxidative stress as biomarkers of premature aging in persons with intellectual disability.

机构信息

Department of Physical Therapy, Sackler Faculty of Medicine, Stanley Steyer School of Health Professions, Tel Aviv University, Ramat Aviv 69978, Israel.

出版信息

Res Dev Disabil. 2012 Mar-Apr;33(2):369-75. doi: 10.1016/j.ridd.2011.10.002. Epub 2011 Nov 25.

DOI:10.1016/j.ridd.2011.10.002
PMID:22119683
Abstract

The decline in cognitive ability and physical performance in older adults with intellectual disabilities (ID) is accompanied by less participation in social activities and a sedentary lifestyle; however the pathogenesis is not clear yet. It was recently suggested that chronic disease, adverse drug reactions, and aging create a cascade of events that can be best characterized as an asymptomatic inflammatory process. This cascade of events is mediated by cytokine interleukins 1 and 6 (IL-1α, and IL-6), nitric oxide (NO) and total oxidative stress (OS). Our hypothesis was that chronic inflammation in the bloodstream of persons with ID contributes to their "premature aging". To test this hypothesis, we measured and compared the levels of inflammatory molecules in persons with and without ID. Fifteen adults with, and 15 adults without ID (control group) participated in this study. The levels of NO metabolites (NOx), IL-1α, and IL-6 were obtained from participants' serum. OS markers were drawn from participants' capillary. Western blot, RT-PCR and specific chemical analysis were used as measurement tools. The levels of inflammatory molecules and OS were significantly higher in persons with ID compared to the control group. Asymptomatic inflammation in the bloodstream of the older adults with ID might explain the "premature aging" of these individuals. Monitoring the levels of inflammatory molecules could serve as biomarkers of "premature aging" which may allow early diagnosis and intervention, and improve the quality of care for persons with ID.

摘要

认知能力和身体机能的下降伴随着智力障碍(ID)老年人社交活动和久坐生活方式的减少;然而,其发病机制尚不清楚。最近有人提出,慢性病、药物不良反应和衰老会引发一连串事件,这些事件最好被描述为一种无症状的炎症过程。这一连串事件是由细胞因子白细胞介素 1 和 6(IL-1α 和 IL-6)、一氧化氮(NO)和总氧化应激(OS)介导的。我们的假设是,ID 患者血液中的慢性炎症导致他们“过早衰老”。为了验证这一假设,我们测量并比较了 ID 患者和无 ID 患者血液中的炎症分子水平。这项研究共纳入了 15 名 ID 患者和 15 名无 ID 的对照组成年人。从参与者的血清中获得了一氧化氮代谢物(NOx)、IL-1α 和 IL-6 的水平,从参与者的毛细血管中获得了 OS 标志物。使用 Western blot、RT-PCR 和特定的化学分析作为测量工具。与对照组相比,ID 患者血液中的炎症分子和 OS 水平显著升高。ID 老年患者血液中的无症状炎症可能解释了这些人的“过早衰老”。监测炎症分子的水平可以作为“过早衰老”的生物标志物,这可能有助于早期诊断和干预,并提高 ID 患者的护理质量。

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