|کد مقاله||کد نشریه||سال انتشار||مقاله انگلیسی||ترجمه فارسی||نسخه تمام متن|
|5736623||1613773||2017||11 صفحه PDF||سفارش دهید||دانلود رایگان|
- BZP reduces the incidence of stroke, neuronal necrosis in the brain.
- BZP inhibits only arachidonic acid (AA) - induced platelet aggregation in vitro.
- BZP inhibits ADP- or thrombin- or AA-induced platelet aggregation ex vivo.
- BZP inhibits thrombus formation in Dahl-SS hypertensive-induced stroke rats.
- BZP could treat and prevent cerebral ischemic stroke in Dahl-SS hypertensive rats.
Our aim was to explore the preventive and therapeutic effects of sodium (Â±)-5-bromo-2-(Î±-hydroxypentyl) benzoate (brand name: brozopine, BZP) on stroke in Dahl Salt-sensitive (Dahl-SS) hypertensive rats. Dahl-SS rats were fed a high-salt diet to observe the effect of BZP on blood pressure, and brain, heart, and kidney tissues. Additionally, the incidence of stroke was recorded according to the neurological score. The relative mechanisms investigated included anti-oxidative effects and anti-platelet aggregation. BZP reduced the incidence of stroke, neuronal necrosis in the brain, and cell swelling and inflammatory infiltration in the kidney. Its mechanisms were related to the increased activities of gluthatione peroxidase and catalase and the decreased level of plasma nitric oxide. BZP inhibited arachidonic acid (AA) - induced platelet aggregation (IC50: 12Â ÂµM) rather than that of adenosine diphosphate (ADP) - and/or thrombin-induced platelet aggregation in vitro. Interestingly, BZP inhibited ADP-, thrombin-, or AA-induced platelet aggregation and elevated the level of AMP-activated protein kinase, cyclic guanosine monophosphate, and vasodilator-stimulated-phosphoprotein, and attenuated ATP contents and mitogen-activated protein kinase levels in platelet and inhibited thrombus formation in a carotid artery thrombosis model, dose-dependently, in Dahl-SS hypertensive-induced stroke rats. In conclusion, BZP can have therapeutic and preventive effects on stroke in Dahl-SS hypertensive rats, the mechanisms of which may be related to anti-oxidant, anti-platelet aggregation and anti-thrombus formation.
Journal: Brain Research - Volume 1672, 1 October 2017, Pages 137-147