Schisandrin B Inhibits Osteoclastogenesis and Protects Against Ovariectomy-Induced Bone Loss
| Autor: | Yimin Dong, Renpeng Peng, Qian Guo, Jia Wang, Zhong Fang, Feng Li, Ya Zhang, Hanfeng Guan, Honglei Kang, Chao Song |
|---|---|
| Rok vydání: | 2020 |
| Předmět: |
0301 basic medicine
MAPK/ERK pathway Pharmacology Schisandrin NF-κB Nrf2 Bone resorption 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Osteoclast medicine Pharmacology (medical) Original Research chemistry.chemical_classification Reactive oxygen species biology lcsh:RM1-950 osteoporosis MAPK In vitro lcsh:Therapeutics. Pharmacology 030104 developmental biology medicine.anatomical_structure chemistry Schisandrin B 030220 oncology & carcinogenesis Mitogen-activated protein kinase osteoclast biology.protein |
| Zdroj: | Frontiers in Pharmacology Frontiers in Pharmacology, Vol 11 (2020) |
| ISSN: | 1663-9812 |
| Popis: | Osteoporosis is a systemic skeletal disease which is highly prevalent worldwide and considered to be associated with excessive bone resorption mediated by osteoclast. Osteoclast differentiation is featured by the activation of inflammation-related pathways and the generation of reactive oxygen species. Schisandrin B is a bioactive compound with strong antiinflammation and antioxidative properties, we thus speculated that Schisandrin B might serve as a potential candidate for osteoporosis. In the present study, we found that the formation and` function of osteoclasts were dramatically suppressed by Schisandrin B. And consistent with the in vitro results, treatment with Schisandrin B attenuated ovariectomy-induced bone loss in mice. Moreover, Schisandrin B notably inhibited the activation of mitogen activated protein kinase (MAPK) and nuclear factor-κB (NF-κB) pathways and scavenged ROS by activating nuclear factor E2 p45-related factor 2 (Nrf2) signaling. In conclusion, our study indicates that Schisandrin B is an effective approach to treat osteoporosis and other osteoclast-related diseases. |
| Databáze: | OpenAIRE |
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