ArticleScientific reports2025
Glaucocalyxin A alleviates ulcerative colitis by inhibiting PI3K/AKT/mTOR signaling.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Intestinal Epithelial Cell Ferroptosis in Ulcerative Colitis: Pathogenesis, Signaling Networks, and Therapeutic Implications.Current medical science · 2026Review
- The role of Traditional Chinese Medicine in the management of liver disease: targeting gut microbiome.Chinese medicine · 2026Review
- Glaucocalyxin A Promotes Spinal Cord Repair By Nrf2/HO-1 Pathway Activation to Suppress AIM2 Inflammasome Formation.Molecular neurobiology · 2026Article
- Integrative Analysis of Intestinal Transcriptomes UnderscoresBioinformatics and biology insights · 2026Article
- Trem2 negatively regulates the MTOR-PKCα axis to protect againstFrontiers in cellular and infection microbiology · 2026Article
- Glaucocalyxin A enhances colonic anastomotic healing after ischemia-reperfusion: experimental findings.Acta cirurgica brasileira · 2026Article
- Harnessing GSK-3β inhibition for lung cancer therapy: emerging opportunities and challenges.Medical oncology (Northwood, London, England) · 2025Review
- Article
- mTOR Signaling in Macrophages: All Depends on the Context.International journal of molecular sciences · 2025Review
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Isodon japonicus (Burm.f.) Hara var. glaucocalyx (Maxim.) Hara is a herbaceous perennial plant. Historically, it has often been used to treat dysentery and other diseases, indicating its potential efficacy in the treatment of inflammatory conditions affecting the intestines. Glaucocalyxin A (GLA) is a diterpenoid isolated from I. japonicus; recent studies have revealed that it exhibits a range of biological activities, including neuroprotective, anticancer, anti-inflammatory, hepatoprotective, and anti-fibrotic effects. However, previous studies have not specifically explored the mechanism whereby GLA alleviates ulcerative colitis (UC). Therefore, in the present study, we generated a DSS-induced UC mouse model and lipopolysaccharide-induced RAW264.7 inflammation model and performed network pharmacology analysis and peripheral blood analysis of patients with acute UC to investigate the mechanisms underlying the positive effects of GLA on UC. This study demonstrated the anti-inflammatory effects of GLA in a mouse model of DSS-induced UC. Network pharmacology analysis revealed that AKT is a common target of GLA and inflammatory bowel disease (IBD). The changes in LPS-induced RAW264.7 cell inflammation further verified that GLA reduced the expression of inflammatory cytokines by inhibiting PI3K/AKT/mTOR signaling. Finally, in vitro magnetic bead sorting experiments showed that GLA could be used in the treatment of UC patients.
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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 Socratic graph.