去卵巢大鼠
破骨细胞
兰克尔
骨吸收
骨质疏松症
化学
NF-κB
磷酸化
内分泌学
骨矿物
内科学
吸收
癌症研究
药理学
信号转导
医学
体外
生物化学
受体
雌激素
激活剂(遗传学)
作者
Qi Zhuang,Shuangshuang Chen,Wei Zhang,Minhui Gu,Long Xiao,Yajun Li,Yunshang Yang,Chengcheng Feng,Hong Li,Dechun Geng,Zhirong Wang
标识
DOI:10.1021/acs.jafc.2c05954
摘要
Osteoporosis (OP) is mainly manifested by bone loss and bone degeneration. OP is considered a risk factor for pathological fractures, as well as impacts the health of middle-aged and elderly individuals. Drug therapy remains the main treatment scheme for OP; however, its efficacy is limited and has been associated with serious side effects. Therefore, it is important to develop new, effective, and safe treatment methods for OP. Avicularin (AL) is a flavonoid and quercetin derivative from various plants. Our study showed that AL disrupts osteoclast activation and resorptive function via inhibition of the RANKL-induced osteoclast differentiation together with the resorption capacity of bone marrow-derived macrophages (BMMs). Hence, AL prevents the activation and resorptive activity of osteoclasts. The results of qPCR showed that genes related to osteoclasts exhibited downregulated expression after AL treatment. Furthermore, AL inhibited RANKL-induced phosphorylation as well as degradation of the inhibitor IκBα of the NF-κB pathway, together with P65 phosphorylation in BMMs. We used an OP mouse model that was established by ovariectomy (OVX). Relative to untreated OP mice, mice that received AL treatment showed a significant increase in bone mineral density; however, the expression of TRAP, NFATC1, mmp9, and CTX-1 was significantly reduced. These results indicate that AL disrupts osteoclastogenesis via inhibition of the NF-κB pathway, which in turn improves OVX-induced OP.
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