详情页 - 广东省中医院知识库

当前位置：首页 > 详情页

Cycloastragenol Attenuates Osteoclastogenesis and Bone Loss by Targeting RANKL-Induced Nrf2/Keap1/ARE, NF-κB, Calcium, and NFATc1 Pathways.

文献详情

资源类型：

Pubmed体系：

作者：

机构： [1]First Affiliated Hospital, Guangzhou University of Chinese Medicine, Guangdong, China, [2]School of Biomedical Sciences, The University of WA, Perth, WA, Australia, [3]Guangzhou University of ChineseMedicine, Guangdong, China, [4]Third Affiliated Hospital, Guangzhou University of Chinese Medicine, Guangdong, China

出处：

DOI：

ISSN：

关键词： cycloastragenol osteoclast RANKL Nfatc1 ROS

摘要：

Osteoporosis, which typically affects postmenopausal women, is an osteolytic disease due to over-activation of osteoclasts. However, current drugs targeting osteoclast inhibition face various side effects, making natural compounds with great interest as alternative treatment options. Cycloastragenol (CAG) is a triterpenoid with multiple biological activities. Previously, CAG's activity against aging-related osteoporosis was reported, but the mechanisms of actions for the activities were not understood. This study demonstrated that CAG dose-dependently inhibited osteoclast formation in receptor activator of nuclear factor-κB ligand (RANKL)-stimulated bone marrow macrophage (BMMs). Mechanism studies showed that CAG inhibited NF-κB, calcium, and nuclear factor of activated T cells 1 (NFATc1) pathways. Additionally, CAG also promoted the nuclear factor-erythroid 2-related factor 2 (Nrf2)/Kelch-like ECH-associated protein 1 (Keap1)/anti-oxidative response element (ARE) pathway that scavenges reactive oxygen species (ROS). Furthermore, CAG was also found to prevent bone loss of postmenopausal osteoporosis (PMO) in a preclinical model of ovariectomized (OVX) mice. Collectively, our research confirms that CAG inhibits the formation and function of osteoclasts by regulating RANKL-induced intracellular signaling pathways, which may represent a promising alternative for the therapy of osteoclast-related disease.Copyright © 2022 Wang, Ma, Chen, Wang, Qiu, Chen, He, Zhang, Guo, Lai, Zhang, Huang, Yang, Yuan, Chen, He and Xu.

语种：

PubmedID：

中科院(CAS)分区：

出版当年[2020]版：

大类 | 2 区医学

小类 | 2 区药学

最新[2025]版：

大类 | 3 区医学

小类 | 3 区药学

第一作者：

第一作者机构： [1]First Affiliated Hospital, Guangzhou University of Chinese Medicine, Guangdong, China, [2]School of Biomedical Sciences, The University of WA, Perth, WA, Australia, [3]Guangzhou University of ChineseMedicine, Guangdong, China,

共同第一作者：

通讯作者：

通讯机构： [3]Guangzhou University of ChineseMedicine, Guangdong, China, [4]Third Affiliated Hospital, Guangzhou University of Chinese Medicine, Guangdong, China

推荐引用方式(GB/T 7714)：

APA：

MLA：

相关文献

[1]Inhibitory Effects of Rhaponticin on Osteoclast Formation and Resorption by Targeting RANKL-Induced NFATc1 and ROS Activity [2]Inhibitory effects of Rhaponticin on osteoclast formation and resorption by targeting RANKL-induced NFATc1 and ROS activity (vol 12, 645140, 2021) [3]A novel RANKL-targeted flavonoid glycoside prevents osteoporosis through inhibiting NFATc1 and reactive oxygen species. [4]A novel Glycyrrhiza glabra extract liquiritin targeting NFATc1 activity and ROS levels to counteract ovariectomy-induced osteoporosis and bone loss in murine model [5]Eriodictyol Inhibits RANKL-Induced Osteoclast Formation and Function Via Inhibition of NFATc1 Activity. [6]Dendrobine attenuates osteoclast differentiation through modulating ROS/NFATc1/MMP9 pathway and prevents inflammatory bone destruction [7]Notopterol Attenuates Estrogen Deficiency-Induced Osteoporosis via Repressing RANKL Signaling and Reactive Oxygen Species. [8]Loureirin B suppresses RANKL-induced osteoclastogenesis and ovariectomized osteoporosis via attenuating NFATc1 and ROS activities. [9]Asiatic Acid Inhibits OVX-Induced Osteoporosis and Osteoclastogenesis Via Regulating RANKL-Mediated NF-κb and Nfatc1 Signaling Pathways. [10]Aconine inhibits RANKL-induced osteoclast differentiation in RAW2647 cells by suppressing NF-κB and NFATc1 activation and DC-STAMP expression

日	一	二	三	四	五	六

今天

清空