维格列汀对正常和STZ诱导的ii型糖尿病大鼠缺血再灌注性脑梗死的抗神经炎作用

K. Purnachander, D. Rao, N. Kannappan
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引用次数: 2

摘要

糖尿病是缺血性脑卒中的主要危险因素之一。糖尿病患者氧化应激基线水平升高会导致脑缺血损伤。在脑缺血再灌注损伤等病理状态下,自由基引起氧化应激和炎症,导致脑损伤加重。炎症是脑缺血再灌注损伤的主要病理机制之一。维格列汀是一类新的抗糖尿病药物DPP-4抑制剂,据报道除了具有抗高血糖活性外,还具有抗炎特性。因此,本研究旨在评价维格列汀对正常和STZ诱导的糖尿病大鼠脑梗死性缺血再灌注损伤的抗炎作用。双侧颈总动脉闭塞后4小时再灌注诱导脑梗死。梗死百分比、炎症标志物如MPO、TNF-?、IL-6和IL-10进行分析。维格列汀治疗4周可显著降低脑梗死体积百分比。10mg /kg剂量的维格列汀显示MPO、TNF-?IL-6和IL-1?与正常组相比,糖尿病组的抗炎标志物如IL-10水平显著增加。维格列汀通过抗炎机制显示出明显的脑保护作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Anti neuroinflammatory effect of Vildagliptin in ischaemia-reperfusion induced cerebral infarction in normal and STZ induced type-II diabetic rats
Diabetes is one of the major risk factor for cerebral ischemic stroke. Increased base line levels of oxidative stress in diabetes will lead to cerebral ischemic damage. In pathological conditions such as cerebral ischemia/reperfusion injury, free radicals cause oxidative stress and inflammation leading to increased injury of brain. Inflammation is one of the major pathological mechanisms involved in cerebral ischemia and reperfusion injury. Vildagliptin newer anti-diabetic drug of the class DPP-4 inhibitors is reported to have anti-inflammatory properties apart from its antihyperglycemic activity. Therefore the aim of the present study is to evaluate the anti-inflammatory effect of Vildagliptin against cerebral infarction induced ischemia reperfusion injury in normal and STZ induced diabetic Wistar rats. Cerebral infarction was induced by bilateral common carotid artery occlusion followed by 4 hr reperfusion. Percent infarction, inflammatory markers such as MPO, TNF-?, IL-6 and IL-10 were analysed. Treatment with Vildagliptin for a period of four weeks produced significant reduction in percent cerebral infarct volume. Vildagliptin at 10 mg/kg dose, showed significant reduction in markers like MPO, TNF-?, IL-6 and IL-1? in diabetic group when compared to normal group and in contrast significant increase in anti-inflammatory marker like IL-10 levels. Vildagliptin showed significant cerebroprotective effect by antiinflammatory mechanisms.
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