Diabetes Care:氧化损伤的DNA/RNA和8-异前列腺素水平与老年2型糖尿病的发生发展有关

2019-10-26 xing.T MedSci原创

由此可见,大型队列研究的结果支持氧化还原系统失衡导致2型糖尿病的发生发展。但提示这种关联仅在年纪较大时才在临床上变得显著,这可能是由于细胞修复能力降低所致。

氧化应激被认为在2型糖尿病的病理生理中起着重要的作用,但是少数评估氧化应激生物标记物与2型糖尿病发生率相关性的队列研究较小型,并且报告的结果尚无定论。

近日,糖尿病领域权威杂志Diabetes Care上发表了一篇研究文章,研究人员以德国未患糖尿病的7828例患者人群为基础评估了尿中氧化鸟嘌呤/鸟苷(OxGua)水平(DNA/RNA氧化的生物标志物)和尿中8-异前列腺素水平(脂质过氧化的生物标志物)与2型糖尿病之间的相关性,该队列研究随访了14年。研究人员使用多变量校正的Cox比例风险回归模型获得每增加1个SD的风险比(HRs)和95%CIs。

在总人群中,OxGua(每增加1个SD的HR[95%CI]为1.05 [1.01; 1.09]和8-异前列腺素(1.04 [1.00; 1.09])的水平与2型糖尿病的发生率存在较弱但有统计学意义的关联。分层分析显示,该队列中最年轻的年龄组(50-59岁)中,这两种生物标志物与2型糖尿病之间的相关性并不存在,而在最高年龄组(65-75岁)中,这两种生物标志物的相关性最强,Gua水平每增加1个SD的HR为1.14(1.05-1.23),8-异前列腺素每增加1个SD的HR为1.22(1.02-1.45)。

由此可见,大型队列研究的结果支持氧化还原系统失衡导致2型糖尿病的发生发展。但提示这种关联仅在年纪较大时才在临床上变得显著,这可能是由于细胞修复能力降低所致。 

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直接暴露于环境的氧化剂和毒物的人体肺组织容易受到伤害,导致急性或慢性氧化损伤。Nrf2(核因子红细胞2相关因子2)代表中枢细胞防御机制,并且是用于开发抗氧化损伤诱导的人类肺部疾病的药物靶标。

Arch Biochem Biophys:ID2通过p-ERK1/2-ID2-NRF2途径保护视网膜色素上皮细胞(RPE)免受氧化损伤

中山大学中山眼科中心眼科国家重点实验室的Fan Y近日在Arch Biochem Biophys发表了一篇文章。他们的研究显示,氧化应激增加了视网膜色素上皮细胞(RPE)中的ID2表达。