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Diabetes:阿司匹林导致II型糖尿病病人过量表达异前列腺素

来源:生物谷 2012-03-27 23:54

II型糖尿病(type 2 diabetes mellitus, T2DM)患者用阿司匹林治疗后,过量表达异前列腺素(isoprostane),而这又会增强招募血小板的能力。相关研究结果于2012年3月16日在线发表在Diabetes期刊上。

因为注意到阿司匹林对II型糖尿病患者的心血管事件有着适度的影响,来自意大利罗马智慧大学(Sapienza University of Rome)的Roberto Cangemi博士和同事们研究了阿司匹林对II型糖尿病患者产生血小板异前列腺素(isoprostane)的影响。他们对50名接受阿司匹林治疗的II型糖尿病患者和50名未接受相应治疗的II型糖尿病患者与100名未患糖尿病的病人在年龄、性别和动脉粥样硬化危险因素和阿司匹林治疗等方面进行比较。

研究人员在糖尿病病人而不是那些未患糖尿病的病人,接受阿司匹林治疗的糖尿病病人而不是未接受相应治疗的糖尿病病人中,观察到更强的血小板招募能力,更高的血小板异前列腺素水平,以及还原型NAD磷酸氧化酶(NAD phosphate oxidase, NOX2)受到激活。在所有接受阿司匹林治疗的病人当中,血小板凝血烷A2(thromboxane A2, TxA2)受到抑制。在这项干预性研究中,研究人员发现在患有糖尿病和未患上糖尿病的那些病人当中,阿司匹林类似地抑制血小板TxA2。在患有糖尿病的病人当中,他们同步观察到血小板招募能力增强,异前列腺素水平增加,NOX2激活,然而在未患有糖尿病的病人当中,他们没有观察到这些变化。

“我们证实II型糖尿病患者服用的低剂量阿司匹林通过上调NOX2产生的活性氧来提高血小板异前列腺素水平”,论文作者们写道,“这种影响减轻阿司匹林产生的抗血小板作用,从而可能解释为什么相比于其他动脉粥样硬化疾病,阿司匹林对II型糖尿病的疗效更低。” (生物谷:towersimper编译)

Platelet Isoprostane Overproduction in Diabetic Patients Treated With Aspirin

Roberto Cangemi, Pasquale Pignatelli, Roberto Carnevale, Carmen Nigro, Marco Proietti, Francesco Angelico, Davide Lauro, Stefania Basili and Francesco Violi

Aspirin modestly influences cardiovascular events in patients with type 2 diabetes mellitus (T2DM), but the reason is unclear. The aim of the study was to determine whether in T2DM patients aspirin enhances platelet isoprostanes, which are eicosanoids with proaggregating properties derived from arachidonic acid oxidation by platelet NOX2, the catalytic subunit of reduced NAD phosphate oxidase. A cross-sectional study was performed comparing T2DM patients, treated (n = 50) or not treated (n = 50) with 100 mg/day aspirin, with 100 nondiabetic patients, matched for age, sex, atherosclerosis risk factors, and aspirin treatment. A short-term (7 days) treatment with 100 mg/day aspirin also was performed in 36 aspirin-free diabetic and nondiabetic patients. Higher platelet recruitment, platelet isoprostane, and NOX2 activation was found in diabetic versus nondiabetic patients and in aspirin-treated diabetic patients versus nontreated patients (P < 0.001). Platelet thromboxane (Tx) A2 (P < 0.001) was inhibited in all aspirin-treated patients. In the interventional study, aspirin similarly inhibited platelet TxA2 in diabetic and nondiabetic patients (P < 0.001). Platelet recruitment, isoprostane levels, and NOX2 activation showed a parallel increase in diabetic patients (P < 0.001) and no changes in nondiabetic patients. These findings suggest that in aspirin-treated diabetic patients, oxidative stress–mediated platelet isoprostane overproduction is associated with enhanced platelet recruitment, an effect that mitigates aspirin-mediated TxA2 inhibition.

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