Corylifol A suppresses osteoclastogenesis and alleviates ovariectomy-induced bone loss via attenuating ROS production and impairing mitochondrial function

骨吸收 PI3K/AKT/mTOR通路 蛋白激酶B 化学 MAPK/ERK通路 兰克尔 骨重建 细胞生物学 磷酸化 骨质疏松症 内分泌学 下调和上调 内科学 癌症研究 信号转导 生物 医学 生物化学 激活剂(遗传学) 受体 基因
作者
HaiShan Li,Wei Deng,Jiamin Yang,Yuewei Lin,ShiYin Zhang,ZiXuan Liang,JunChun Chen,MinHua Hu,Teng Liu,Guo‐ye Mo,Zhen Zhang,DongPing Wang,Peng Gu,YongChao Tang,Kai Yuan,Liangliang Xu,Jiake Xu,Shuncong Zhang,YongXian Li
出处
期刊:Biomedicine & Pharmacotherapy [Elsevier]
卷期号:171: 116166-116166 被引量:1
标识
DOI:10.1016/j.biopha.2024.116166
摘要

Osteoporosis is a systemic disease characterized by an imbalance in bone homeostasis, where osteoblasts fail to fully compensate for the bone resorption induced by osteoclasts. Corylifol A, a flavonoid extracted from Fructus psoraleae, has been identified as a potential treatment for this condition. Predictions from network pharmacology and molecular docking studies suggest that Corylifol A exhibits strong binding affinity with NFATc1, Nrf2, PI3K, and AKT1. Empirical evidence from in vivo experiments indicates that Corylifol A significantly mitigates systemic bone loss induced by ovariectomy by suppressing both the generation and activation of osteoclasts. In vitro studies further showed that Corylifol A inhibited the activation of PI3K-AKT and MAPK pathways and calcium channels induced by RANKL in a time gradient manner, and specifically inhibited the phosphorylation of PI3K, AKT, GSK3 β, ERK, CaMKII, CaMKIV, and Calmodulin. It also diminishes ROS production through Nrf2 activation, leading to a decrease in the expression of key regulators such as NFATcl, C-Fos, Acp5, Mmp9, and CTSK that are involved in osteoclastogenesis. Notably, our RNA-seq analysis suggests that Corylifol A primarily impacts mitochondrial energy metabolism by suppressing oxidative phosphorylation. Collectively, these findings demonstrate that Corylifol A is a novel inhibitor of osteoclastogenesis, offering potential therapeutic applications for diseases associated with excessive bone resorption.
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