ArticleDrug design, development and therapy2016
Celastrol inhibits prostaglandin E2-induced proliferation and osteogenic differentiation of fibroblasts isolated from ankylosing spondylitis hip tissues in vitro.
Article in Drug design, development and therapy, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 31 citations in OpenAlex.
- Comprehensive overview of alternative medicine in the treatment of ankylosing spondylitis: Symptoms, pathogenesis, diagnosis and treatments (Review).Biomedical reports · 2026Review
- Fibroblasts in heterotopic ossification: mechanisms and therapeutic targets.International journal of biological sciences · 2025Review
- TRAIL and Celastrol Combinational Treatment Suppresses Proliferation, Migration, and Invasion of Human Glioblastoma Cells via Targeting Wnt/β-catenin Signaling Pathway.Chinese journal of integrative medicine · 2024Article
- Exploring hub pyroptosis-related genes, molecular subtypes, and potential drugs in ankylosing spondylitis by comprehensive bioinformatics analysis and molecular docking.BMC musculoskeletal disorders · 2023Article
- MYC promotes fibroblast osteogenesis by regulating ALP and BMP2 to participate in ectopic ossification of ankylosing spondylitis.Arthritis research & therapy · 2023Article
- Fibroblast Insights into the Pathogenesis of Ankylosing Spondylitis.Journal of inflammation research · 2023Review
- Circ_0018168 inhibits the proliferation and osteogenic differentiation of fibroblasts in ankylosing spondylitis via regulating miR-330-3p/DKK1 axis.Regenerative therapy · 2022Article
- A mechanistic review of chinese medicine polyphenols on bone formation and resorption.Frontiers in pharmacology · 2022Review
- Anti-Osteogenic Effect of Danshensu in Ankylosing Spondylitis: AnFrontiers in pharmacology · 2021Article
- MicroRNA‑204‑5p inhibits the osteogenic differentiation of ankylosing spondylitis fibroblasts by regulating the Notch2 signaling pathway.Molecular medicine reports · 2020Article
- Micheliolide alleviates ankylosing spondylitis (AS) by suppressing the activation of the NLRP3 inflammasome and maintaining the balance of Th1/Th2 via regulating the NF-κB signaling pathway.Annals of translational medicine · 2020Article
- miR-17-5p Regulates Heterotopic Ossification by Targeting ANKH in Ankylosing Spondylitis.Molecular therapy. Nucleic acids · 2019Article
- Prostaglandin receptor EP4 expression by Th17 cells is associated with high disease activity in ankylosing spondylitis.Arthritis research & therapy · 2019Article
- Clinical and MRI response to dose reduction of an etanercept-biosimilar for hip arthritis in patients with ankylosing spondylitis: an observational, retrospective cohort study.Clinical rheumatology · 2019Observational
- MiR-495 targeting dvl-2 represses the inflammatory response of ankylosing spondylitis.American journal of translational research · 2019Article
- Emodin induces apoptosis and autophagy of fibroblasts obtained from patient with ankylosing spondylitis.Drug design, development and therapy · 2019Article
- Dissecting the Underlying Pharmaceutical Mechanism of Chinese Traditional Medicine Yun-Pi-Yi-Shen-Tong-Du-Tang Acting on Ankylosing Spondylitis through Systems Biology Approaches.Scientific reports · 2017Article
- Celastrol: A Spectrum of Treatment Opportunities in Chronic Diseases.Frontiers in medicine · 2017Review
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHeterotopic ossification on the enthesis, which develops after subsequent inflammation, is one of the most distinctive features in ankylosing spondylitis (AS). Prostaglandin E2 (PGE-2) serves as a key mediator of inflammation and bone remodeling in AS. Celastrol, a well-known Chinese medicinal herb isolated from Tripterygium wilfordii, is widely used in treating inflammatory diseases, including AS. It has been proven that it can inhibit lipopolysac-charide-induced expression of various inflammation mediators, such as PGE-2. However, the mechanism by which celastrol inhibits inflammation-induced bone forming in AS is unclear.
objectiveTo investigate whether celastrol could inhibit isolated AS fibroblast osteogenesis induced by PGE-2.
methodsHip synovial tissues were obtained from six AS patients undergoing total hip replacement in our hospital. Fibroblasts were isolated, primarily cultured, and then treated with PGE-2 for osteogenic induction. Different doses of celastrol and indometacin were added to observe their effects on osteogenic differentiation. Cell proliferation, osteogenic markers, alizarin red staining as well as the activity of alkaline phosphatase were examined in our study.
resultsCelastrol significantly inhibits cell proliferation of isolated AS fibroblasts and in vitro osteogenic differentiation compared with control groups in a time- and dose-dependent manner.
conclusionOur results demonstrated that celastrol could inhibit isolated AS fibroblast proliferation and in vitro osteogenic differentiation. The interaction of PI3K/AKT signaling and Wnt protein may be involved in the process. Further studies should be performed in vivo and animal models to identify the potential effect of celastrol on the bone metabolism of AS patients.
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