ReferenceID 6031
Plumbagin relieves rheumatoid arthritis through nuclear factor kappa-B (NF-κB) pathway
Bioengineered
This study aimed to explore the effects of plumbagin on rheumatoid arthritis (RA) and its mechanism. The RA cell model was simulated following the treatment of interleukin-1β (IL-1β). After the treatment of various conce
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Record Fields
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- Reference Id
- 6031
- Evidence Id
- 22621
- Core Evidence Id
- 22621
- Source Reference Id
- 5325
- Herb2 Reference Id
- HBREF006122
- Subject Paper Key
- HBIN040266_35653787
- Pubmed Id
- 35653787
- Doi
- 10.1080/21655979.2022.2081756
- Paper Title
- Plumbagin relieves rheumatoid arthritis through nuclear factor kappa-B (NF-κB) pathway
- Paper Abstract
- This study aimed to explore the effects of plumbagin on rheumatoid arthritis (RA) and its mechanism. The RA cell model was simulated following the treatment of interleukin-1β (IL-1β). After the treatment of various concentrations of plumbagin, the impact of plumbagin on the cell viability was examined by 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The collagen-induced arthritis (CIA) model was established using the solution of bovine type II collagen. Hematoxylin-eosin staining was used to observe the changes of ankle joint tissue, while enzyme-linked immunosorbent assay and western blot were applied to detect the level of inflammatory cytokines. Plumbagin inhibited the viability of human fibroblast-like synoviocytes (HFLS) at the concentration of 1 ~ 3.5 μM. The inhibitory effect of 1 μM plumbagin on cell proliferation was similar to that of methotrexate, the drug used as the positive control. Plumbagin downregulated the levels of inflammatory cytokines and matrix metalloproteinases (MMPs) in IL-1β-treated HFLS, and suppressed the activation of IκB and nuclear factor kappa-B (NF-κB) as well as the entry of p65 into the nucleus. It was also demonstrated in animal experiments that plumbagin inhibited the activation of NF-κB pathway, down-regulated the levels of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and MMPs, and alleviated joint damage in CIA-modeled mice. Collectively speaking, plumbagin might down-regulate the levels of inflammatory cytokines and MMPs through inhibiting the activation of the NF-κB pathway, thereby attenuating RA-induced damage to cells and joints. Abbreviations : CIA: Collagen-induced arthritis; ELISA: Enzyme-linked immuno sorbent assay; HFLS: Human fibroblast-like synoviocytes; IL-6: Interleukin-6; IL-1β: Interleukin-1β; NF-κB: nuclear factor kappa-B; MTT: 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide; MMPs: Matrix metalloproteinase; OD: Optical density; RA: Rheumatoid arthritis; SDS: Sodium dodecyl sulfate; SD: Standard deviation; TNF-α: Tumor necrosis factor-α; PVDF: Polyvinylidene fluoride.
- Journal
- Bioengineered
- Publish Year
- 2022
- Experiment Subject
- mouse; human; bovine; ra cell model
- Experiment Type
- Cell Experiment
- Phenotype Related
- Arthritis; Rheumatoid Arthritis; Collagen-induced Arthritis; Tumor
- Paper Title Cn
- Paper Title En
- Plumbagin relieves rheumatoid arthritis through nuclear factor kappa-B (NF-κB) pathway
- Bilingual Status
- semi_complete