Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2022
Stachydrine exhibits a novel antiplatelet property and ameliorates platelet-mediated thrombo-inflammation.
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.
Sun Xianting, Zhou Meng, Pu Jun, Wang Ting
Аннотация
BACKGROUND: Platelets are versatile anucleate cells involved in thrombosis as well as inflammation. Stachydrine (STA), a major bioactive compound extracted from Motherwort, has multiple pharmacological properties. Nevertheless, the significance of STA in platelet regulation and whether STA could ameliorate platelet-mediated thrombo-inflammation still remain elusive.
METHODS: Human platelets were used to assess the regulatory effects of STA on platelet activation and interactions with neutrophils in vitro. FeCl3 injury-induced carotid/mesenteric thrombosis and collagen/epinephrine-induced pulmonary thromboembolism model were used to explore whether STA could regulate thrombosis in vivo. Furthermore, a cecal ligation and puncture-induced sepsis model was employed to investigate the role of STA in thrombo-inflammatory diseases.
RESULTS: STA markedly suppressed platelet activation represented by aggregation, secretion, αIIbβ3-mediated signaling events and calcium mobilization, etc. by inhibiting agonists-induced activation signaling and potentiating cGMP-dependent inhibitory signaling. Mice receiving STA-treated platelets were less susceptible to thrombosis in vivo. In addition, decreased platelet-neutrophil interactions including platelet-neutrophil aggregates and neutrophil extracellular traps, and alleviative sepsis-induced multiorgan damage were observed due to STA-mediated platelet inhibition.
CONCLUSION: This study suggested the potential therapeutic role of STA in thrombotic and thrombo-inflammatory disorders.
METHODS: Human platelets were used to assess the regulatory effects of STA on platelet activation and interactions with neutrophils in vitro. FeCl3 injury-induced carotid/mesenteric thrombosis and collagen/epinephrine-induced pulmonary thromboembolism model were used to explore whether STA could regulate thrombosis in vivo. Furthermore, a cecal ligation and puncture-induced sepsis model was employed to investigate the role of STA in thrombo-inflammatory diseases.
RESULTS: STA markedly suppressed platelet activation represented by aggregation, secretion, αIIbβ3-mediated signaling events and calcium mobilization, etc. by inhibiting agonists-induced activation signaling and potentiating cGMP-dependent inhibitory signaling. Mice receiving STA-treated platelets were less susceptible to thrombosis in vivo. In addition, decreased platelet-neutrophil interactions including platelet-neutrophil aggregates and neutrophil extracellular traps, and alleviative sepsis-induced multiorgan damage were observed due to STA-mediated platelet inhibition.
CONCLUSION: This study suggested the potential therapeutic role of STA in thrombotic and thrombo-inflammatory disorders.