含笑内酯的药理作用及机制研究进展
x

请在关注微信后,向客服人员索取文件

篇名: 含笑内酯的药理作用及机制研究进展
TITLE: Research progress on pharmacological effects and mechanism of micheliolide
摘要: 含笑内酯是一种来自天然植物的愈创木烷型倍半萜内酯,在木兰科植物黄兰及台湾含笑的根皮中均有分布。现代药理学研究表明,含笑内酯可通过抑制肿瘤细胞增殖、调节肿瘤细胞凋亡、诱导肿瘤细胞自噬、抑制肿瘤细胞的侵袭和转移等发挥抗肿瘤作用;其可通过调控核因子κB、磷脂酰肌醇-3-羟激酶/蛋白激酶B等多条相关信号通路,降低炎症细胞因子的表达水平;其可通过恢复机体免疫相关因子表达,发挥免疫调节作用;其可通过减少β淀粉样蛋白的积累、抑制小胶质细胞活化等发挥神经保护作用;其可通过减轻肝细胞的炎症反应和脂肪变性等发挥肝脏保护作用;其肾脏保护作用机制与其可通过调控多个通路来减轻炎症反应有关;其心脏保护作用机制包括减轻炎症反应,降低氧化应激水平等。总之,含笑内酯是一种具有重要开发价值的化合物。
ABSTRACT: Micheliolide is a kind of guaiacane sesquiterpene lactone from natural plants. It distributs in the root bark of Cephalantheropsis gracilis and Michelia compressa . Modern pharmacological studies show that ,micheliolide can play an anti-tumor role by inhibiting the proliferation of tumor cells ,regulating the apoptosis of tumor cells ,inducing autophagy of tumor cells ,and inhibiting invasion and metastasis of tumor cells. It can reduce the expression of inflammatory cytokines by regulating several related signaling pathways ,such as nuclear factor κB and phosphatidylinositol-3-hydroxykinase/protein kinase B ;it can play an immunomodulatory role by restoring the expression of immune-related factors in the body ;it can play a neuroprotective effect by reducing the accumulation of amyloid β-protein and inhibiting microglial activation ;it can play a liver protective role by reducing the inflammatory response and steatosis of hepatocytes ;its nephroprotective mechanism is related to the relief of the inflammatory response by regulating multiple pathways ;the mechanisms of its cardioprotective action include alleviating the inflammatory response and reducing the level of oxidative stress ,etc. In conclusion ,micheliolide is a compound of great development value.
期刊: 2022年第33卷第14期
作者: 林景,莫俊俏,周欣,宋艳,黎咏嫦
AUTHORS: LIN Jing,MO Junqiao ,ZHOU Xin,SONG Yan,LI Yongchang
关键字: 含笑内酯;药理作用;机制;抗肿瘤;抗炎;免疫调节;神经保护
KEYWORDS: micheliolide;pharmacological effects ;mechanism;anti-tumor;anti-inflammatory;immune regulation ;nerve
阅读数: 376 次
本月下载数: 12 次

* 注:未经本站明确许可,任何网站不得非法盗链资源下载连接及抄袭本站原创内容资源!在此感谢您的支持与合作!