依达拉奉对烟酰胺链脲佐菌素致糖尿病大鼠脑出血后氧化蛋白修饰及明胶酶活性的影响

A. Lievykh, V. Zhyliuk, V. Tkachenko, Y. Kharchenko, G. Ushakova, A. Shevtsova
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摘要

中风,尤其是出血性中风,是糖尿病最严重的合并症之一,通常与高死亡率相关,特别是2型糖尿病(T2DM)。因此,寻找具有代谢保护作用的药物是相关的。依达拉奉(Edaravone, Eda)被广泛用于缺血性脑卒中的治疗,但其在2型糖尿病脑出血(intracarhemorrhage, ICH)中的生化作用尚未得到证实。本研究的目的是评估Eda对实验性T2DM大鼠在胶原酶诱导的脑出血后氧化修饰蛋白(OMP)标志物的影响,如晚期氧化蛋白产物(AOPP)、中性和碱性羰基(PC370和PC430)、晚期糖基化终产物(AGE)和缺血修饰白蛋白(IMA),以及基质金属蛋白酶MMP2/MMP9(明胶酶)活性的影响。二甲双胍被用作比较药物。所得数据表明,糖尿病大鼠的ICH伴随着AOPP、PC370、AGE以及两种明胶酶成熟形式的增加。而脑出血后IMA和proMMP9均低于正常水平。两种药物都将OMP标记物降低到正常大鼠的水平或更低,Eda显示出更有效的效果。此外,Eda显著降低了MMP9的活性,改变了前胶酶的活性。我们得出的结论是,Eda通过抑制氧化应激和调节明胶酶活性,在治疗T2DM共病性脑出血方面有一定的应用前景。
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Effects of edaravone on oxidative protein modification and activity of gelatinases after intracerebral hemorrhage in rats with nicotinamide-streptozotocin induced diabetes
Stroke, especially hemorrhagic form, is one of the most serious comorbidity disease of diabetes mellitus, often associated with high mortality, particularly in type 2 DM (T2DM). Therefore, it is relevant the search for drugs with a metabolically justified protective effect. Edaravone (Eda) is widely used for treating ischemic stroke but its biochemical effects in intracerebral hemorrhage (ICH) associated with T2DM is not still confirmed. The aim of the study was to assess the impact of Eda on the markers of oxidative modification of proteins (OMP), such as advanced oxidation protein products (AOPP), neutral and basic carbonyls (PC370 and PC430), advanced glycation end products (AGE) and ischemia modified albumin (IMA) as well as on the activity of matrix metalloproteinases MMP2/MMP9 (gelatinases) in rats with experimental T2DM after collagenase-induced ICH. Metformin was used as a comparative drug. The data obtained indicate that ICH in diabetic rats is accompanied by an increase in AOPP, PC370, AGE, and mature forms of both gelatinases. On the contrary, IMA and proMMP9 were below normal level after ICH. Both studied drugs decreased the OMP markers to the levels of intact rats or lower, and Eda show a more potent effect. Besides, Eda significantly decreased the activity of MMP9 and changed progelatinases activity. We conclude that Eda has a perspective to be useful in the treatment of comorbid brain hemorrhage in T2DM due to inhibiting of oxidative stress and modulation of gelatinases activity.
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