ReferenceID 2256

Maackiain dampens osteoclastogenesis via attenuating RANKL-stimulated NF-κB signalling pathway and NFATc1 activity

J Cell Mol Med

Osteolytic diseases are typified by over-enhanced formation and resorbing function of osteoclasts and have a major impact on human health. Inhibition of osteoclastic differentiation and function is a key strategy for cli

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Reference Id
2256
Evidence Id
18846
Core Evidence Id
18846
Source Reference Id
4550
Herb2 Reference Id
HBREF005347
Subject Paper Key
HBIN034075_32939977
Pubmed Id
32939977
Doi
10.1111/jcmm.15647
Paper Title
Maackiain dampens osteoclastogenesis via attenuating RANKL-stimulated NF-κB signalling pathway and NFATc1 activity
Paper Abstract
Osteolytic diseases are typified by over-enhanced formation and resorbing function of osteoclasts and have a major impact on human health. Inhibition of osteoclastic differentiation and function is a key strategy for clinical therapy of osteolytic conditions. Maackiain is a natural compound extracted from Sophora flavescens, which has been applied to anti-allergic and anti-tumour treatments. The present results showed that Maackiain could restrain receptor activator of nuclear factor-kappaB ligand (RANKL)-stimulated osteoclast formation and hydroxyapatite resorption dose-dependently, and interrupt the structures of F-actin belts in the mature osteoclasts. It also repressed the expressions of osteoclast-specific genes and proteins. Furthermore, Maackiain could inhibit RANKL-stimulated NF-kappaB and calcium signalling pathways, and dampen Nuclear factor of activated T cell cytoplasmic 1 activity, protein expression and translocation into the nucleus. These results revealed that Maackiain may have a potential therapeutic effect on osteoclast-related disorders.
Journal
J Cell Mol Med
Publish Year
2020
Experiment Subject
human
Experiment Type
Cell Experiment
Phenotype Related
Osteolytic Conditions; Osteoclast-related Disorders; Osteolytic Diseases
Paper Title Cn
Paper Title En
Maackiain dampens osteoclastogenesis via attenuating RANKL-stimulated NF-κB signalling pathway and NFATc1 activity
Bilingual Status
semi_complete