Kaempferol Prevents Against Ang II-induced Cardiac Remodeling Through Attenuating Ang II-induced Inflammation and Oxidative Stress
Kaempferol Prevents Against Ang II-induced Cardiac Remodeling Through Attenuating Ang II-induced Inflammation and Oxidative Stress
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DOI：
10.1097/fjc.0000000000000713
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发表时间：
2019-10-01
影响因子：
3
通讯作者：
Ge, Weihong
中科院分区：
文献类型：
--
作者：
Du, Yao;Han, Jibo;Ge, Weihong
以心脏重构为特征的心力衰竭是一个全球性问题。血管紧张素II（Ang II）诱导心脏炎症和氧化应激，这也涉及不良胶原积聚诱导的重塑的病理生理学。山奈酚（Kaempferol，KPF）是一种黄酮类化合物，具有抗炎和抗氧化活性。然而，科索沃爱国阵线的目标仍然模糊不清。在这项研究中，我们研究了KPF对血管紧张素II诱导的胶原积累的影响，并探讨了潜在的机制。我们的研究结果表明，KPF预防Ang II诱导的心脏纤维化和功能障碍，在小鼠皮下注射Ang II的挑战。在培养细胞中，KPF显着减少血管紧张素II诱导的胶原积累。此外，KPF通过调节NF-κ B B/丝裂原活化蛋白激酶和AMPK/Nrf 2通路，显著降低Ang II刺激的心脏成纤维细胞的炎症和氧化应激。
Heart failure characterized by cardiac remodeling is a global problem. Angiotensin II (Ang II) induces cardiac inflammation and oxidative stress, which also is implicated in the pathophysiology of adverse collagen accumulation-induced remodeling. Kaempferol (KPF), a kind of flavonoid compounds, is capable of anti-inflammatory and antioxidant activities. However, the target of KPF still remains blurred. In this study, we investigated the effect of KPF on Ang II-induced collagen accumulation and explored the underlying mechanisms. Our results suggested that KPF prevented Ang II-induced cardiac fibrosis and dysfunction, in mice challenged with subcutaneous injection of Ang II. In culture cells, KPF significantly reduced Ang II-induced collagen accumulation. Furthermore, KPF remarkably decreased inflammation and oxidative stress in Ang II-stimulated cardiac fibroblasts by modulating NF-kappa B/mitogen-activated protein kinase and AMPK/Nrf2 pathways.