评估一种重氮辛因衍生物对缺血再灌注损伤模型心力衰竭的生物学活性。
Evaluation of Biological Activity of a Diazocine Derivative against Heart Failure Using an Ischemia-Reperfusion Injury Model.
机构信息
Laboratory of Pharmaco-Chemistry, Faculty of Chemical Biological Sciences, University Autonomous of Campeche, Campeche, México.
Facultad de Nutrición, Universidad Veracruzana, Médicos y Odontologos s/n, Unidad del Bosque, Veracruz, México.
出版信息
Drug Res (Stuttg). 2022 Sep;72(7):404-411. doi: 10.1055/a-1840-3199. Epub 2022 Jun 20.
BACKGROUND
There are studies, which suggest that some diazocine derivatives can exert effects on the cardiovascular system; however, these effects are not very clear.
OBJECTIVE
The aim of this research was to evaluate the biological activity of a diazocine derivative against heart failure translated as area infarct.
METHODS
Biological activity produced by diazocine derivatives against heart failure was determinate using an ischemia/reperfusion injury model. Besides, to characterize the molecular mechanism of effect exerted by diazocine derivative on left ventricular pressure (LVP) was determinate in an isolated rat heart model using nifedipine, PINAME TXA, and quinalizarin as controls.
RESULTS
The results showed that diazocine derivative decrease the infarct area and increase the LVP. However, the effect produced by diazocine derivative on LVP was inhibited in the presence of quinalizarin.
CONCLUSIONS
The results indicate that biological activity produced by diazocine derivative on left ventricular pressure is through protein CK2 activation; this phenomenon could be translated as a decrease in both infarct area and heart failure.
背景
有研究表明，一些重氮嗪衍生物对心血管系统有一定作用，但作用机制尚不清楚。
目的
本研究旨在评价重氮嗪衍生物对心力衰竭的生物学活性。
方法
采用缺血/再灌注损伤模型，测定重氮嗪衍生物对心力衰竭的生物学活性。此外，用硝苯地平、PINAME TXA 和奎纳克林作为对照，在离体大鼠心脏模型中，测定重氮嗪衍生物对左心室压（LVP）的作用机制。
结果
结果表明，重氮嗪衍生物可减少梗死面积，增加 LVP。然而，奎纳克林的存在抑制了重氮嗪衍生物对 LVP 的作用。
结论
结果表明，重氮嗪衍生物对左心室压的生物学活性是通过蛋白 CK2 的激活产生的；这种现象可能表现为梗死面积和心力衰竭的减少。
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