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脑源性神经营养因子在大鼠全身炎症反应模型中抵消了白细胞介素-2的心脏保护作用。

Brain-Derived Neurotrophic Factor Cancels the Cardioprotective Effect of Interleukin-2 in a Model of Systemic Inflammatory Response in Rats.

作者信息

Burovenko I Yu, Borshchev Yu Yu, Minasyan S M, Protsak E S, Borshcheva O V, Galagudza M M

机构信息

Almazov National Medical Research Center, Ministry of Health of the Russian Federation, St. Petersburg, Russia.

Petrov National Medical Research Center of Oncology, Ministry of Health of the Russian Federation, St. Petersburg, Russia.

出版信息

Bull Exp Biol Med. 2025 Mar;178(5):577-580. doi: 10.1007/s10517-025-06377-z. Epub 2025 Apr 29.

Abstract

Contradictory data about the cardioprotective and neuroprotective effects of IL-2 and BDNF and our own data on specific differences in myocardial resistance to ischemia-reperfusion after administration of exogenous IL-2 and BDNF prompted us to study the effect of combined administration of these two agents on the size of the necrosis zone in the isolated heart of rats with modeled systemic inflammatory response syndrome (SIRS). In the SIRS group, a significant increase in most proinflammatory markers in the blood and a 65% increase in the area of myocardial necrosis after ischemia-reperfusion in comparison with the control were observed. After IL-2 administration, the necrosis zone was significantly smaller than in rats with SIRS and the level of most analytes decreased. Combined administration of IL-2 and BDNF abolished the decrease in the size of the necrosis zone compared to that in rats with SIRS.

摘要

关于白细胞介素 -2(IL -2)和脑源性神经营养因子(BDNF)的心脏保护和神经保护作用存在相互矛盾的数据,以及我们自己关于外源性IL -2和BDNF给药后心肌对缺血再灌注耐受性的特定差异的数据,促使我们研究这两种药物联合给药对模拟全身性炎症反应综合征(SIRS)大鼠离体心脏坏死区大小的影响。在SIRS组中,观察到与对照组相比,血液中大多数促炎标志物显著增加,缺血再灌注后心肌坏死面积增加65%。给予IL -2后,坏死区明显小于SIRS大鼠,大多数分析物水平降低。与SIRS大鼠相比,IL -2和BDNF联合给药消除了坏死区大小的减小。

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