葛根素
化学
活力测定
西妥因1
药理学
氧化应激
细胞凋亡
丙二醛
炎症体
上睑下垂
细胞毒性
乳酸脱氢酶
免疫印迹
锡尔图因
流式细胞术
生物化学
分子生物学
下调和上调
程序性细胞死亡
体外
酶
医学
生物
替代医学
病理
基因
受体
NAD+激酶
作者
X. Li,Y. Li,Huihui Jiao,AiTing Wang,Man Zheng,ChunYan Xiang,FengLei Zhang
摘要
Abstract Puerarin (Pue) has significant antioxidant and anti‐inflammatory properties. This work was designed to clarify and investigate the potential mechanisms of Pue in atherosclerosis (AS) progression. In vivo, acrolein (Acr) was inhaled through drinking water to construct AS model. In vitro, CCK‐8 assay and lactate dehydrogenase (LDH) assay kit were used to detect cell viability. Apoptosis was detected by flow cytometry. The content of malondialdehyde (MDA) was determined by commercial kit, the level of inflammatory factors was detected by ELISA, and proteins were determined by western blot. Pue administration could effectively reduce blood lipid level in Acr‐fed mice. Pue suppressed oxidative stress, the formation of atherosclerotic plaques, and the process of aortic histological changes. Pue pretreatment decreased MDA in HUVECs and maintained the activity of antioxidant enzymes. Pue upregulated SIRT1/Nrf2 cascade in HUVECs. Pue increased MYH9 and inhibited NLRP3 inflammasome‐related proteins, and the inhibition of MYH9 significantly impaired Pue‐induced Nrf2 activation. Moreover, HUVEC cytotoxicity and apoptosis are alleviated by Pue, in addition to NLRP3‐mediated pyroptosis in HUVECs induced by Acr. MYH9 inhibitors effectively suppressed the pyroptosis induced by Acr and prevented injury to HUVECs. In addition, Pue promoted SIRT1/Nrf2 cascade activation in HUVECs. Pue may alleviate Acr‐induced AS by activating the MYH9‐mediated SIRT1/Nrf2 cascade to inhibit inflammasome activation.
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