ArticleExploration (Beijing, China)2025
Saikosaponin b1 Attenuates Liver Fibrosis by Blocking STAT3/Gli1 Interaction and Inducing Gli1 Degradation.
Article in Exploration (Beijing, China), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Targeting eEF1A1 With Baicalein to Block eEF1A1/Prdx4 Interaction for Treating Sepsis-Mediated Lung Injury.Exploration (Beijing, China) · 2026Article
- Clearing the Pulmonary Traffic Jam With Dual-Enzyme Inhalable Nanoparticles Restore Airflow and Reverse Fibrotic Remodeling.Advanced healthcare materials · 2026Article
- Metal-drug coordinated nanozymes for ROS scavenging and Kupffer cell polarization to alleviate drug-induced liver injury.Acta pharmaceutica Sinica. B · 2026Article
- Article
- Targeted intestinal delivery of luteolin microcapsules as a precision nutritional strategy to alleviate heat stress and enhance growth performance in broilers.Poultry science · 2026Article
- Design, Synthesis, and Antiviral Evaluation of Novel 3,4-Dihydropyrimidin-2(1Microorganisms · 2026Article
- The enhanced photothermal therapy against gastric cancer by mitochondria/STAT3-targeted nanoplatform with OXPHOS blocking.Materials today. Bio · 2026Article
- Therapeutic Potential of Saikosaponins in MASLD and Cross-Organ Protection: A Research Update.Food science & nutrition · 2026Review
- Multiorgan repair by MSC-derived extracellular vesicles in hepatorenal syndrome through necroptosis alleviation, immune reprogramming and fibrosis resolution.Extracellular vesicles and circulating nucleic acids · 2026Article
- Saikosaponin b1 Attenuates Liver Fibrosis by Blocking STAT3/Gli1 Interaction and Inducing Gli1 Degradation.Exploration (Beijing, China) · 2025Article
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16 authors.
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Abstract
Saikosaponin b1 (Ssb1), a natural oleanane-type triterpenoid saponin, exhibits antifibrosis activity by inhibiting the activation of hepatic stellate cells (HSCs), but the specific underlying molecular mechanisms are unknown. Here, it is found that Ssb1 could directly bind with the signal transducer and activator of transcription 3 (STAT3) and effectively inhibit the activation of HSCs. Proteomic techniques and molecular simulation revealed that Ssb1 is mainly bound to the S319 residues of STAT3 in the coiled-coil domain. Further studies indicated that Ssb1 binding with STAT3 inhibited its transcriptional activity, and regulated glioma-associated oncogene-1 (Gli1) expression in the Hedgehog signaling pathway. Besides, Ssb1 binding blocked interaction between STAT3 and Gli1, which promoted degradation of Gli1 protein by suppressor of fused homolog (SUFU) and the ubiquitin-proteasome system. The loss function of Gli1 led to decreased expression of Bcl2 and promoted the apoptosis of activated HSCs. Moreover, STAT3 ablation abolished the Ssb1-mediated antifibrotic effects. These findings show that STAT3 plays a vital role in Ssb1 treatment of liver fibrosis, and Ssb1 as a STAT3 inhibitor might be a promising therapeutic candidate for the treatment of hepatic fibrosis.
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