自噬
PI3K/AKT/mTOR通路
蛋白激酶B
细胞生物学
下调和上调
化学
信号转导
活性氧
药理学
生物
细胞凋亡
生物化学
基因
作者
Zhenhui Luo,Ao Zeng,Yuankun Chen,Shumiao He,Siqing He,Xiaobao Jin,Chunmei Li,Wenjie Mei,Qun Lu
标识
DOI:10.1016/j.ejphar.2021.174184
摘要
Autophagy is essential to vessel homeostasis and function in the cardiovascular system. Ligustilide (LIG) is one of the main active ingredients extracted from traditional Chinese medicines, such as Ligusticum chuanxiong, Angelica, and other umbelliferous plants, and reported to have cardiovascular protective effects. In this study, we explore the effects and the potential mechanism of ligustilide on the Ang II-induced autophagy in A7r5 cells. Our results showed that ligustilide inhibited the Ang II-induced autophagy in A7r5 cells and down regulated the expression of autophagy-related proteins LC3, ULK1, and Beclin-1. Ligustilide exerted a protective effect on the reduction of the concentrations of reactive oxygen species and Ca2+ and upregulated the nitric oxide concentration in A7r5 cells with Ang II-induced autophagy. Additionally, the analyses of network pharmacological targets and potential signal pathways indicated that the target of ligustilide to regulate autophagy was related to the Akt/mTOR signaling pathway. Furthermore, ligustilide could upregulate the expression of p-Akt and p-mTOR and inhibit the expression of LC3II in A7r5 cells with Ang II-induced autophagy. These findings showed that ligustilide inhibited the autophagic flux in A7r5 cells induced by Ang II via the activation of the Akt/mTOR signaling pathway.
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