잠시만 기다려 주세요. 로딩중입니다.

콜라겐-유도의 사람 혈소판에서 PI3K/Akt 및 MAPK 조절을 통한 Isoscopoletin의 항혈소판 효과

Anti-platelet Effects of Isoscopoletin through Regulation of PI3K/Akt and MAPK on Collagen-induced Human Platelets

생약학회지 2020년 51권 3호 p.151 ~ 157
이동하,
소속 상세정보
이동하 ( Lee Dong-Ha ) - Namseoul University Department of Biomedical Laboratory Science

Abstract


When blood vessels are damaged, a rapid hemostatic reaction occurs to minimize blood loss and maintain normal circulation. Platelet activation and aggregation is essential in this process. However, excessive platelet aggregation or abnormal platelet aggregation may be the cause of cardiovascular disease, such as thrombosis, stroke and atherosclerosis. Therefore, it is important to prevent and treat cardiovascular disease by finding substances that can regulate platelet activation and suppress aggregation reactions. Isoscopoletin, which is mainly found in the roots of plants Artemisia or Scopolia, has been reported to have potential pharmacological effects on anticancer and Alzheimer’s disease, but its role and mechanisms for platelet aggregation and thrombus formation are unknown. This study confirmed the effect of isoscopoletin on major regulation of collagen-induced human platelet aggregation, TXA2 production and intracellular granular secretion (ATP and serotonin release). In addition, the effects of isoscopoletin on phosphorylation of phosphorylated proteins PI3K/Akt and MAPK involved in signal transduction in platelet aggregation was studied. As a result, isoscopoletin significantly inhibited the phosphorylation of PI3K/Akt and MAPK, significantly inhibiting platelet aggregation through TXA2 production and intracellular granular secretion (ATP and serotonin release). Therefore, we suggest that isoscopoletin is an anti-platelet substance that regulates phosphorylation of phosphorus proteins such as PI3K/Akt and MAPK and is valuable as a preventive and therapeutic agent for platelet-derived cardiovascular disease.

키워드

Isoscopoletin; PI3K/Akt; MAPK; TXA2; Granule secretion

원문 및 링크아웃 정보

 

등재저널 정보