ReferenceID 4957
Corilagin suppresses RANKL-induced osteoclastogenesis and inhibits oestrogen deficiency-induced bone loss via the NF-κB and PI3K/AKT signalling pathways
J Cell Mol Med
Over-activated osteoclastogenesis, which is initiated by inflammation, has been implicated in osteoporosis. Corilagin, a natural compound extracted from various medicinal herbaceous plants, such as Cinnamomum cassia, has
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Record Fields
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- Reference Id
- 4957
- Evidence Id
- 21547
- Core Evidence Id
- 21547
- Source Reference Id
- 3165
- Herb2 Reference Id
- HBREF003962
- Subject Paper Key
- HBIN021473_32681612
- Pubmed Id
- 32681612
- Doi
- 10.1111/jcmm.15657
- Paper Title
- Corilagin suppresses RANKL-induced osteoclastogenesis and inhibits oestrogen deficiency-induced bone loss via the NF-κB and PI3K/AKT signalling pathways
- Paper Abstract
- Over-activated osteoclastogenesis, which is initiated by inflammation, has been implicated in osteoporosis. Corilagin, a natural compound extracted from various medicinal herbaceous plants, such as Cinnamomum cassia, has antioxidant and anti-inflammatory activities. We found that Corilagin suppressed osteoclast differentiation in a dose-dependent manner, significantly decreased osteoclast-related gene expression and impaired bone resorption by osteoclasts. Moreover, phosphorylation of members of the nuclear factor-kappaB (NF-kappaB) and PI3K/AKT signalling pathways was reduced by Corilagin. In a murine model of osteoporosis, Corilagin inhibited osteoclast functions in vivo and restored oestrogen deficiency-induced bone loss. In conclusion, our findings suggested that Corilagin inhibited osteoclastogenesis by down-regulating the NF-kappaB and PI3K/AKT signalling pathways, thus showing its potential possibility for the treatment of osteoporosis.
- Journal
- J Cell Mol Med
- Publish Year
- 2020
- Experiment Subject
- mouse
- Experiment Type
- Animal Experiment
- Phenotype Related
- Oestrogen Deficiency; Osteoporosis
- Paper Title Cn
- Paper Title En
- Corilagin suppresses RANKL-induced osteoclastogenesis and inhibits oestrogen deficiency-induced bone loss via the NF-κB and PI3K/AKT signalling pathways
- Bilingual Status
- semi_complete