Diabetes:新型降糖药或可减少卒中后脑损伤

2012-12-11 Diabetes Diabetes

       在小鼠中开展的一项研究中,瑞典卡罗林斯卡医学院的科学家们发现了一种新的潜在疗法,可能减少2型糖尿病患者卒中后的脑损伤。所建议的药物已获批准用于2型糖尿病的治疗。然而,科学家们希望,这一新的研究成果,也可能开辟了减少其他卒中高风险患者卒中发作后脑损伤的可能性。该项研究已在线发表于Diabetes期刊[Diabetes 2012 Dec 3]。

       在小鼠中开展的一项研究中,瑞典卡罗林斯卡医学院的科学家们发现了一种新的潜在疗法,可能减少2型糖尿病患者卒中后的脑损伤。所建议的药物已获批准用于2型糖尿病的治疗。然而,科学家们希望,这一新的研究成果,也可能开辟了减少其他卒中高风险患者卒中发作后脑损伤的可能性。该项研究已在线发表于Diabetes期刊[Diabetes 2012 Dec 3]。

       然而,这种疗法仅适合于10%的卒中患者,同时具有潜在的严重副作用,主要是脑出血。此外,溶栓治疗的效果在糖尿病患者中会降低,这是因为糖尿病本身可导致一种敏感的血管结构。

       该项研究的基础是一种化学物质,名为linagliptin(利拉利汀片,商品名为
Trajenta),该药已商业化用于糖尿病的治疗。结合运动及特殊饮食,linagliptin能够降低2型糖尿病患者的血糖水平。在这项研究中,在诱导卒中试验前后,科学家们将linagliptin或安慰剂给药糖尿病小鼠。通过采用该研究的设计,科学家模拟了2型糖尿病患者接受linagliptin治疗的情景。

       结果表明,linagliptin能够激发神经保护,同时在很大程度上减少卒中后脑损
伤,这种作用独立于该药的降糖效果。这反过来表明,2型糖尿病患者中,当给与linagliptin治疗,在卒中后可能比接受其他药物具有更好的预后。

       Linagliptin是一种二肽基肽酶–4(DPP-4)抑制剂,是勃林格殷格翰公司的原研
产品,已获美国、欧盟、日本、印度等国批准,作为2型糖尿病患者饮食和运动治疗的一种辅助治疗,用以改善血糖控制。



Abstract
Type 2 diabetes is a strong risk factor for stroke. Linagliptin is a dipeptidyl peptidase-4 (DPP-4) inhibitor in clinical use against type 2 diabetes. The aim of this study was to determine the potential antistroke efficacy of linagliptin in type 2 diabetic mice. To understand whether efficacy was mediated by glycemia regulation, a comparison with the sulfonylurea glimepiride was done. To determine whether linagliptin-mediated efficacy was dependent on a diabetic background, experiments in nondiabetic mice were performed. Type 2 diabetes was induced by feeding the mice a high-fat diet for 32 weeks. Mice were treated with linagliptin/glimepiride for 7 weeks. Stroke was induced at 4 weeks into the treatment by transient middle cerebral artery occlusion. Blood DPP-4 activity, glucagon-like peptide-1 (GLP-1) levels, glucose, body weight, and food intake were assessed throughout the experiments. Ischemic brain damage was measured by determining stroke volume and by stereologic quantifications of surviving neurons in the striatum/cortex. We show pronounced antistroke efficacy of linagliptin in type 2 diabetic and normal mice, whereas glimepiride proved efficacious against stroke in normal mice only. These results indicate a linagliptin-mediated neuroprotection that is glucose-independent and likely involves GLP-1. The findings may provide an impetus for the development of DPP-4 inhibitors for the prevention and treatment of stroke in diabetic patients.

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