ArticleExperimental biology and medicine (Maywood, N.J.)2018
The effects of dihydroartemisinin on inflammatory bowel disease-related bone loss in a rat model.
Article in Experimental biology and medicine (Maywood, N.J.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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13 citing papers in PubMed, 24 citations in OpenAlex.
- Huanglian-Wendan Decoction alleviates DSS-induced colitis by modulating the gut microbiota and protecting against intestinal injury via suppression of colonic apoptosis and endoplasmic reticulum stress.Natural products and bioprospecting · 2026Article
- Cross-talk of gut-bone-muscle: osteosarcopenia in experimental colitis models.Laboratory animal research · 2026Review
- Dihydroartemisinin enhances remyelination by switching microglia to the reparative phenotype.Journal of neuroinflammation · 2025Article
- Dihydroartemisinin ameliorates hemarthrosis-induced cartilage degeneration by suppressing chondrocyte senescence via activation of Keap1-Nrf2 signaling pathway.Journal of orthopaedic translation · 2025Article
- Therapeutic Potential of BMP7 in the Treatment of Osteoporosis Caused by the Interaction between Inflammation and Corticosteroids in Inflammatory Bowel Disease.Biomedicines · 2023Article
- Engineered procyanidin-Fe nanoparticle alleviates intestinal inflammation through scavenging ROS and altering gut microbiome in colitis mice.Frontiers in chemistry · 2023Article
- Mechanism and Prospect of Gastrodin in Osteoporosis, Bone Regeneration, and Osseointegration.Pharmaceuticals (Basel, Switzerland) · 2022Review
- Probiotics Stimulate Bone Formation in Obese Mice via Histone Methylations.Theranostics · 2021Article
- Dihydroartemisinin: A Potential Drug for the Treatment of Malignancies and Inflammatory Diseases.Frontiers in oncology · 2021Review
- Effects of emodin on inflammatory bowel disease-related osteoporosis.Bioscience reports · 2020Article
- Dihydroartemisinin Regulates the Th/Treg Balance by Inducing Activated CD4+ T cell Apoptosis via Heme Oxygenase-1 Induction in Mouse Models of Inflammatory Bowel Disease.Molecules (Basel, Switzerland) · 2019Article
- Histone Deacetylases Enhance CaInternational journal of molecular sciences · 2018Article
- Meta-analysis of proteomics data from osteoblasts, bone, and blood: Insights into druggable targets, active factors, and potential biomarkers for bone biomaterial design.Journal of tissue engineeringArticle
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6 authors at 4 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Bone loss is one of the important extra-intestinal manifestations in patients with inflammatory bowel diseases (IBDs). Compounds derived from natural products have been used to treat IBDs. However, the role of natural products on IBD-induced bone loss is not completely clarified. In the present study, we observed the effects of dihydroartemisinin (DHA), an antimalaria drug, on IBD and IBD-induced bone loss in a rat model. Chronic IBD model was established in Sprague-Dawley rats by giving them 2.5% dextran sodium sulfate in drinking water. DHA was given by intraperitoneal injection. Blood, colon, and bone samples were collected for biomarker assay and histological analysis. There was an obvious increase in tumor necrotic factor (TNF) α and receptor activator of nuclear factor (NF)-kB ligand (RANKL), and decrease in procollagen type 1 N-terminal propeptide (P1NP) level in IBD groups compared with the normal control (p < 0.05). The disease activity score of IBD rats was significantly higher than the control (p < 0.01). Obvious decrease in disease activity score, TNFα, and RANKL level and increase in P1NP were observed in DHA-treated IBD rats. Bone loss, shown as the decrease in bone mineral density, bone volume fraction, and trabecular number and increase in trabecular separation were observed in IBD rats compared with control (p < 0.01). DHA treatment obviously abolished the bone loss, in particular in the high-dose group (p < 0.05). DHA treatment also inhibited the excessive osteoclast formation; RANKL protein expression; and RANK, TRAF6, Fra-1, NFATc1 mRNA expression induced by IBD. Our data indicated that DHA may be a potential therapeutic agent for IBD and IBD-induced bone loss. Impact statement Bone loss is one of the important extra-intestinal manifestations in patients with inflammatory bowel diseases (IBDs). Studies have shown that compounds derived from natural products are useful in the treatment of IBDs. However, few studies have investigated the role of compounds derived from natural products in treatment of osteoporosis in IBDs. The current study aimed to show the effects of dihydroartemisinin (DHA), antimalaria drug, on bone loss in a rat model of IBD. The findings showed that DHA intervention dose dependently protected against bone loss in IBD rats by inhibiting tumor necrotic factor α production and osteoclast formation. These findings highlights that DHA may be beneficial for bone health in those patients with IBD.
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