ReferenceID 4473
Alpinetin ameliorates bone loss in LPS-induced inflammation osteolysis via ROS mediated P38/PI3K signaling pathway
Pharmacol Res
Background and objective: Bone loss occurs in several inflammatory diseases because of chronic persistent inflammation that activates osteoclasts (OCs) to increase bone resorption. Currently available antiresorptive drug
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Record Fields
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- Reference Id
- 4473
- Evidence Id
- 21063
- Core Evidence Id
- 21063
- Source Reference Id
- 2231
- Herb2 Reference Id
- HBREF003028
- Subject Paper Key
- HBIN015751_35988868
- Pubmed Id
- 35988868
- Doi
- 10.1016/j.phrs.2022.106400
- Paper Title
- Alpinetin ameliorates bone loss in LPS-induced inflammation osteolysis via ROS mediated P38/PI3K signaling pathway
- Paper Abstract
- Background and objective: Bone loss occurs in several inflammatory diseases because of chronic persistent inflammation that activates osteoclasts (OCs) to increase bone resorption. Currently available antiresorptive drugs have severe side effects or contraindications. Herein, we explored the effects and mechanism of Alpinetin (Alp) on receptor activator of nuclear factor κB ligand (RANKL)-mediated OCs differentiation, function, and in inflammatory osteolysis of mice. Method: Primary mouse bone marrow-derived macrophages (BMMs) induced by RANKL and macrophage colony-stimulating factor (M-CSF) were utilized to test the impact of Alp on OCs differentiation, function, and intracellular reactive oxygen species (ROS) production, respectively. Expression of oxidant stress relevant factors and OCs specific genes were assessed via real-time quantitative PCR. Further, oxidative stress-related factors, NF-κB, MAPK, PI3K/AKT/GSK3-β, and NFATc1 pathways were examined via Western blot. Finally, LPS-induced mouse calvarial osteolysis was used to investigate the effect of Alp on inflammatory osteolysis in vivo. Result: Alp suppressed OCs differentiation and resorption function, and down-regulated the ROS production. Alp inhibited IL-1β, TNF-α and osteoclast-specific gene transcription. It also blocked the gene and protein expression of Nox1 and Keap1, but enhanced Nrf2, CAT, and HO-1 protein levels. Additionally, Alp suppressed the phosphorylation of PI3K and P38, and restrained the expression of osteoclast-specific gene Nfatc1 and its auto-amplification, hence minimizing LPS-induced osteolysis in mice. Conclusion: Alp is a novel candidate or therapeutics for the osteoclast-associated inflammatory osteolytic ailment.
- Journal
- Pharmacol Res
- Publish Year
- 2022
- Experiment Subject
- mouse; primary mouse bone marrow-derived macrophages
- Experiment Type
- Animal & Cell Experiment
- Phenotype Related
- Inflammatory Diseases; Osteoclast-associated Inflammatory Osteolytic Ailment; Calvarial Osteolysis; Chronic Persistent Inflammation; Inflammatory Osteolysis; Osteolysis
- Paper Title Cn
- Paper Title En
- Alpinetin ameliorates bone loss in LPS-induced inflammation osteolysis via ROS mediated P38/PI3K signaling pathway
- Bilingual Status
- semi_complete