European journal of pharmacology · 2025
Peroxiredoxin 2 alleviates myocardial ischemia-reperfusion injury by inhibiting platelet activity via the AKT/NF-κB pathway.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Gu Chengying, Chen Qian, Wang Liang, Qian Hao, Tian Ran, Liu Zhenyu, Zhang Shuyang
Аннотация
BACKGROUND: Platelet activation is a key factor that aggravates the prognosis of myocardial ischemia-reperfusion injury (MIRI). Peroxiredoxin 2 (Prdx2) is an endogenous peroxidase that helps mitigate atherosclerosis and myocardial infarction; however, its effect on platelets in MIRI remains unclear.
METHODS: Prdx2 expression and platelet activation status were assessed in patients with acute coronary syndrome (ACS) and stable angina pectoris (SAP). Then, the effect of Prdx2 on agonist-induced platelet activation and MIRI was assessed by using the rat MIRI model. SC79 (an AKT pathway activator) was used to reveal the underlying mechanisms.
RESULTS: Patients with ACS had lower serum Prdx2 levels than those with SAP. Rats pretreated with Prdx2 exhibited reduced levels of creatine kinase-myocardial band (CK-MB) and lactate dehydrogenase (LDH). HE staining revealed that Prdx2 alleviated myocardial necrosis and inflammatory infiltration in MIRI rats. Prdx2-pretreated rats revealed improved cardiac systolic function compared to the sham controls. 2,3,5-triphenyltetrazolium chloride staining demonstrated that the MIRI was attenuated by Prdx2 pretreatment. When compared to sham controls, Prdx2 pretreatment platelets exhibited inhibition in platelet aggregation, Adenosine Triphosphate (ATP) release, P-selectin and αIIbβ3 expression, spreading area on fibrinogen, and in vivo hemostatic function. SC79 partially attenuated the above-mentioned platelet inhibition and cardioprotection of Prdx2. Protein blotting experiments of platelets revealed that Prdx2 inhibited AKT/NF-κB phosphorylation in MIRI, which SC79 reversed.
CONCLUSION: Prdx2 inhibited platelet activation and ameliorated MIRI by inhibiting AKT/NF-κB phosphorylation in platelets.
METHODS: Prdx2 expression and platelet activation status were assessed in patients with acute coronary syndrome (ACS) and stable angina pectoris (SAP). Then, the effect of Prdx2 on agonist-induced platelet activation and MIRI was assessed by using the rat MIRI model. SC79 (an AKT pathway activator) was used to reveal the underlying mechanisms.
RESULTS: Patients with ACS had lower serum Prdx2 levels than those with SAP. Rats pretreated with Prdx2 exhibited reduced levels of creatine kinase-myocardial band (CK-MB) and lactate dehydrogenase (LDH). HE staining revealed that Prdx2 alleviated myocardial necrosis and inflammatory infiltration in MIRI rats. Prdx2-pretreated rats revealed improved cardiac systolic function compared to the sham controls. 2,3,5-triphenyltetrazolium chloride staining demonstrated that the MIRI was attenuated by Prdx2 pretreatment. When compared to sham controls, Prdx2 pretreatment platelets exhibited inhibition in platelet aggregation, Adenosine Triphosphate (ATP) release, P-selectin and αIIbβ3 expression, spreading area on fibrinogen, and in vivo hemostatic function. SC79 partially attenuated the above-mentioned platelet inhibition and cardioprotection of Prdx2. Protein blotting experiments of platelets revealed that Prdx2 inhibited AKT/NF-κB phosphorylation in MIRI, which SC79 reversed.
CONCLUSION: Prdx2 inhibited platelet activation and ameliorated MIRI by inhibiting AKT/NF-κB phosphorylation in platelets.