Therapeutic Effects of Salvianolic Acid B on Angiotensin II-Induced Atrial Fibrosis by Regulating Atrium Metabolism via Targeting AMPK/FoxO1/miR-148a-3p Axis.
Therapeutic Effects of Salvianolic Acid B on Angiotensin II-Induced Atrial Fibrosis by Regulating Atrium Metabolism via Targeting AMPK/FoxO1/miR-148a-3p Axis.
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丹酚酸 B 通过靶向 AMPK/FoxO1/miR-148a-3p 轴调节心房代谢对血管紧张素 II 诱导的心房纤维化的治疗作用
DOI：
10.1007/s12265-022-10303-3
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发表时间：
2023-04
影响因子：
3.4
通讯作者：
Zhang, Daoliang
中科院分区：
文献类型：
--
作者：
Liu, Jie;Sun, Qijuan;Sun, Xiaotong;Wang, Qian;Zou, Guangchen;Wang, Dewei;Zhuang, Baoxiang;Juan, Zhaodong;Zhang, Rui;Zhang, Daoliang
本研究从代谢组学的角度探讨了丹参素B（SalB）对血管紧张素II（Ang II）激活的心房成纤维细胞的作用及其可能机制。代谢谱分析对Ang II和对照组进行了最佳分离，表明Sal B对Ang II激活的成纤维细胞（FB）具有恢复作用。我们发现Ang II + Sal B组的代谢物水平逆转至正常。此外，还鉴定了23种重要代谢产物。代谢网络分析表明这些代谢产物参与了嘌呤代谢和FoxO信号通路。我们发现Sal B激活AMP活化蛋白激酶（AMPK）磷酸化，进而促进FoxO 1的活化，增加miR-148 a-3 p水平。我们进一步证实，Sal B调节异常AMP，磷酸肌酸，谷胱甘肽（GSH），和活性氧（ROS）的生产在血管紧张素II刺激的FB。Sal B可通过AMPK/FoxO 1/miRNA-148 a-3 p轴保护Ang II激活的FB免受纤维化和氧化应激的影响。
The present study highlights the effects of salvianolic acid B (Sal B) on angiotensin II (Ang II)–activated atrial fibroblasts as well as the associated potential mechanism from the metabonomics perspective. Metabolic profile analysis performed an optimal separation of the Ang II and control group, indicating a recovery impact of Sal B on Ang II–activated fibroblasts (FBs). We found that metabolite levels in the Ang II + Sal B group were reversed to normal. Moreover, 23 significant metabolites were identified. Metabolic network analysis indicated that these metabolites participated in purine metabolism and FoxO signaling pathway. We found that Sal B activated AMP-activated protein kinase (AMPK) phosphorylation, which further promoted FoxO1 activation and increased miR-148a-3p level. We further verified that Sal B modulate the abnormal AMP, phosphocreatine, glutathione (GSH), and reactive oxygen species (ROS) production in Ang II–stimulated FBs. Collectively, Sal B can protect the Ang II–activated FBs from fibrosis and oxidative stress via AMPK/FoxO1/miRNA-148a-3p axis.
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