ArticleNaunyn-Schmiedeberg's archives of pharmacology2025
Astragaloside IV regulates macrophage polarization via the TLR4/NF-κB/STAT3 pathway to inhibit the malignant phenotype of renal clear cell carcinoma.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Osteoimmunomodulation of astragalus-calcium silicate scaffolds-activated M2 macrophage-derived miR-218-rich exosome for enhanced bone regeneration.Materials today. Bio · 2025Article
- Astragaloside IV: a potential nemesis for gastric cancer.Frontiers in pharmacology · 2025Review
- Acetylation in renal physiology and pathophysiology.Frontiers in pharmacology · 2025Review
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Clear cell renal cell carcinoma (ccRCC) is a common and aggressive type of kidney cancer. This study aimed to investigate the effect of astragaloside IV (AS-IV) on ccRCC. A variety of cell experimental techniques were used, inducing macrophage polarization, and detecting relevant indicators by flow cytometry, qRT-PCR, immunofluorescence, MTT, wound healing, Transwell, and western blot. A nude mouse xenograft tumor model was constructed for in vivo studies, and siRNA interference technology was used to explore the signaling pathway. The results demonstrated successful macrophage polarization, with AS-IV inhibiting M2 macrophage polarization and promoting the transition from M0 to M1 polarization. Additionally, AS-IV suppressed ccRCC cell proliferation, migration, and invasion, while reversing the malignant effects of M2 macrophages. The study further revealed that AS-IV inhibited M2 polarization through the TLR4/NF-κB/STAT3 signaling pathway. In vivo experiments showed that AS-IV inhibited the growth of ccRCC tumors. This study revealed that AS-IV influences macrophage polarization by regulating the TLR4/NF-κB/STAT3 signaling pathway, thereby inhibiting the malignant phenotype of ccRCC. This finding provides new insights and potential therapeutic strategies for the treatment of ccRCC.
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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.