ArticleEvidence-based complementary and alternative medicine : eCAM2014
Anti-inflammatory and antiosteoclastogenic activities of parthenolide on human periodontal ligament cells in vitro.
Article in Evidence-based complementary and alternative medicine : eCAM, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 34 citations in OpenAlex.
- Parthenolide ameliorates glucocorticoid-induced inhibition of osteogenic differentiation and osteoporosis by activating ERK signaling pathway.Journal of orthopaedic surgery and research · 2025Article
- Review
- A Comparison between BulgarianMolecules (Basel, Switzerland) · 2024Article
- Alternatives to β-Lactams as Agents for the Management of Dentoalveolar Abscess.Current topics in medicinal chemistry · 2024Review
- The therapeutic effect and mechanism of parthenolide in skeletal disease, cancers, and cytokine storm.Frontiers in pharmacology · 2023Review
- The Role of Inflammasome NLPR3 in the Development and Therapy of Periodontitis.International journal of medical sciences · 2022Review
- Chemical Constituents ofEvidence-based complementary and alternative medicine : eCAM · 2021Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Periodontitis is an inflammatory disease that causes osteolysis and tooth loss. It is known that the nuclear factor kappa B (NF-κB) signalling pathway plays a key role in the progression of inflammation and osteoclastogenesis in periodontitis. Parthenolide (PTL), a sesquiterpene lactone extracted from the shoots of Tanacetum parthenium, has been shown to possess anti-inflammatory properties in various diseases. In the study reported herein, we investigated the effects of PTL on the inflammatory and osteoclastogenic response of human periodontal ligament-derived cells (hPDLCs) and revealed the signalling pathways in this process. Our results showed that PTL decreased NF-κB activation, I-κB degradation, and ERK activation in hPDLCs. PTL significantly reduced the expression of inflammatory (IL-1β, IL-6, and TNF-α) and osteoclastogenic (RANKL, OPG, and M-CSF) genes in LPS-stimulated hPDLCs. In addition, PTL attenuated hPDLC-induced osteoclastogenic differentiation of macrophages (RAW264.7 cells), as well as reducing gene expression of osteoclast-related markers in RAW264.7 cells in an hPDLC-macrophage coculture model. Taken together, these results demonstrate the anti-inflammatory and antiosteoclastogenic activities of PTL in hPDLCs in vitro. These data offer fundamental evidence supporting the potential use of PTL in periodontitis treatment.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.