Journal: Chinese Medicine

Article Title: Ginsenoside Rb1 targets the NRF2-PPARγ-ACSL4 axis to inhibit PTECs ferroptosis

doi: 10.1186/s13020-025-01292-x

Figure Lengend Snippet: Rb1 attenuated the progression of AKI and improves the inflammatory response in IRI-induced AKI mice. Animals were divided into: Sham group, Rb1 group, IRI group and Rb1 + IRI group. A The scheme of IRI-induced AKI model and Rb1 treatment. B , C BUN and blood CREA levels in mice. n = 6. D Representative images for H&E and PAS staining in kidneys (magnification ×400, scale bar 200 μm). E Tubular injury scores of H&E and PAS staining. n = 6. F Relative mRNA expression of NGAL and Kim-1. n = 6. G Relative mRNA expression of TNF-α, IL-1β, IL-6 and MCP. n = 6. *P < 0.05, compared with Sham group; #P < 0.05, compared with IRI group

Article Snippet: Ginsenoside Rb1 (#HY-N0039), RSL3 (#HY-100218A) and Ferrostatin-1 (Fer-1, #HY-100579) were purchased from MedChemExpress (Monmouth Junction, USA).

Techniques: Staining, Expressing

Journal: Chinese Medicine

Article Title: Ginsenoside Rb1 targets the NRF2-PPARγ-ACSL4 axis to inhibit PTECs ferroptosis

doi: 10.1186/s13020-025-01292-x

Figure Lengend Snippet: Rb1 inhibits ferroptosis in IRI-induced AKI mice. A Heatmap showing DEGs in the different groups assayed by RNA-seq. B Volcano plot displaying DEGs in Rb1 + IRI group compared with IRI group. C Enrichment analysis of KEGG signaling enriched pathways in Rb1 + IRI group compared with IRI group. D , E Western bolt results and quantitative analysis of GPX4, SLC7A11, TFRC and FTH1. n = 6. F Relative mRNA expression of GPX4, SLC7A11, TFRC and FTH1. n = 6. G – I GSH, MDA and ferrous iron levels of kidney tissue. n = 6. *P < 0.05, compared with Sham group; #P < 0.05, compared with IRI group

Article Snippet: Ginsenoside Rb1 (#HY-N0039), RSL3 (#HY-100218A) and Ferrostatin-1 (Fer-1, #HY-100579) were purchased from MedChemExpress (Monmouth Junction, USA).

Techniques: RNA Sequencing, Western Blot, Expressing

Journal: Chinese Medicine

Article Title: Ginsenoside Rb1 targets the NRF2-PPARγ-ACSL4 axis to inhibit PTECs ferroptosis

doi: 10.1186/s13020-025-01292-x

Figure Lengend Snippet: Rb1 inhibits ferroptosis in RSL3-induced HK-2 cells. A Cell viability assayed by CCK-8. n = 3. B – D Ferrous iron, GSH, and MDA levels of HK-2 cells. n = 3. E – I Western bolt results and quantitative analysis of GPX4, SLC7A11, TFRC and FTH1. n = 3. J Representative transmission electron microscopy pictures of HK-2 cells and quantification of relative mitochondrial length (scale bar 1 μm). n = 3. K , L Representative photomicrographs and quantitative analysis of HK-2 cells stained with DCFH-DA fluorescent probe (magnification ×40, scale bar 200 μm). n = 3. M Relative mRNA expression of GPX4, SLC7A11, TFRC and FTH1. n = 3. *P < 0.05, compared with NC group; #P < 0.05, compared with RSL3 group; &P < 0.05, compared with RSL3 + Rb1 group

Article Snippet: Ginsenoside Rb1 (#HY-N0039), RSL3 (#HY-100218A) and Ferrostatin-1 (Fer-1, #HY-100579) were purchased from MedChemExpress (Monmouth Junction, USA).

Techniques: CCK-8 Assay, Western Blot, Transmission Assay, Electron Microscopy, Staining, Expressing

Journal: Chinese Medicine

Article Title: Ginsenoside Rb1 targets the NRF2-PPARγ-ACSL4 axis to inhibit PTECs ferroptosis

doi: 10.1186/s13020-025-01292-x

Figure Lengend Snippet: PPARγ and ACSL4 were the core gene in Rb1-mediated ferroptosis inhibition. A GSEA showing the increased PPAR signaling pathway enrichment in Rb1 + IRI group compared with IRI group. B Heatmap displaying ferroptosis related DEGs from RNA-seq data. C – E Western bolt results and quantitative analysis of PPARγ and ACSL4 in vivo. n = 6. F – I Relative mRNA expression of PPARγ and ACSL4 in vivo and vitro. J – L Western bolt results and quantitative analysis of PPARγ and ACSL4 in vitro. n = 3. N , M Representative photomicrographs and quantitative analysis of HK-2 cells stained with C11-Bodipy fluorescent probe (magnification ×100, scale bar 200 μm). n = 3. *P < 0.05, compared with Sham group or with NC group; #P < 0.05, compared with IRI group or with RSL3 group; &P < 0.05, compared with RSL3 + Rb1 group

Article Snippet: Ginsenoside Rb1 (#HY-N0039), RSL3 (#HY-100218A) and Ferrostatin-1 (Fer-1, #HY-100579) were purchased from MedChemExpress (Monmouth Junction, USA).

Techniques: Inhibition, RNA Sequencing, Western Blot, In Vivo, Expressing, In Vitro, Staining

Journal: Chinese Medicine

Article Title: Ginsenoside Rb1 targets the NRF2-PPARγ-ACSL4 axis to inhibit PTECs ferroptosis

doi: 10.1186/s13020-025-01292-x

Figure Lengend Snippet: NRF2 was the key transcription factor in Rb1-mediated ferroptosis inhibition. A Flow chart showing the process of network pharmacology analysis. B Venn diagram illustrating the overlapped targets identified among Rb1, AKI, and ferroptosis. C PPI network displaying the top 15 core targets. D Molecular docking and docking scores of Rb1 to the catalytic core of NRF2. E (a) Root mean square deviation (RMSD), (b) root mean square fluctuation (RMSF), (c) Radius of gyration (Rg), (d) Hydrogen bond counts, and (e) solvent-accessible surface area (SASA) curves of the NRF2-Rb1 complex. F Free energy landscape of the NRF2-Rb1 complex. G Structural comparison of the NRF2-Rb1 complex at six time points (0, 20, 40, 60, 80, 100 ns) during molecular dynamics simulations. H Per-residue energy decomposition analysis of NRF2 residues involved in Rb1 binding. I CETSA-Western blot analysis showed the protection of NRF2 by Rb1 at different temperature gradients (n = 3). *P < 0.05, compared with NC group

Article Snippet: Ginsenoside Rb1 (#HY-N0039), RSL3 (#HY-100218A) and Ferrostatin-1 (Fer-1, #HY-100579) were purchased from MedChemExpress (Monmouth Junction, USA).

Techniques: Inhibition, Solvent, Comparison, Residue, Binding Assay, Western Blot

Journal: Chinese Medicine

Article Title: Ginsenoside Rb1 targets the NRF2-PPARγ-ACSL4 axis to inhibit PTECs ferroptosis

doi: 10.1186/s13020-025-01292-x

Figure Lengend Snippet: NRF2 as a key regulator modulating PPARγ in Rb1-conferred anti-ferroptosis. A – F Western bolt results, its quantitative analysis and relative mRNA expression of NRF2 in vivo and vitro. G Binding motifs of NRF2 from the JASPAR database. H ChIP assay analysis of NRF2 binding to PPARγ in HK-2 cells treated with or without RSL3 and Rb1. *P < 0.05, compared with Sham group or with NC group; #P < 0.05, compared with IRI group or with RSL3 group; &P < 0.05, compared with RSL3 + Rb1 group

Article Snippet: Ginsenoside Rb1 (#HY-N0039), RSL3 (#HY-100218A) and Ferrostatin-1 (Fer-1, #HY-100579) were purchased from MedChemExpress (Monmouth Junction, USA).

Techniques: Western Blot, Expressing, In Vivo, Binding Assay

Journal: Chinese Medicine

Article Title: Ginsenoside Rb1 targets the NRF2-PPARγ-ACSL4 axis to inhibit PTECs ferroptosis

doi: 10.1186/s13020-025-01292-x

Figure Lengend Snippet: ML385 abolished the NRF2-PPARγ-ACSL4 axis and the anti-ferroptosis effect of Rb1. A – F Western bolt results and quantitative analysis of GPX4, SLC7A11, NRF2, PPARγ and ACSL4 in vitro. n = 3. G – I Relative mRNA expression of NRF2, PPARγ and ACSL4 in vitro. n = 3. *P < 0.05, compared with NC group; #P < 0.05, compared with RSL3 group; &P < 0.05, compared with RSL3 + Rb1 group

Article Snippet: Ginsenoside Rb1 (#HY-N0039), RSL3 (#HY-100218A) and Ferrostatin-1 (Fer-1, #HY-100579) were purchased from MedChemExpress (Monmouth Junction, USA).

Techniques: Western Blot, In Vitro, Expressing

Journal: Chinese Medicine

Article Title: Ginsenoside Rb1 targets the NRF2-PPARγ-ACSL4 axis to inhibit PTECs ferroptosis

doi: 10.1186/s13020-025-01292-x

Figure Lengend Snippet: Schematic diagram illustrating the protective role of Rb1 in IRI-induced AKI and its underlying mechanism. GinsenosideRb1 downregulates ACSL4 expression through the NRF2-PPARγ-ACSL4 signaling pathway, thereby inhibiting lipid peroxidation and ferroptosis, which ultimately alleviates IRI-induced AKI (parts of the figure were drawn by using pictures from SciDraw)

Article Snippet: Ginsenoside Rb1 (#HY-N0039), RSL3 (#HY-100218A) and Ferrostatin-1 (Fer-1, #HY-100579) were purchased from MedChemExpress (Monmouth Junction, USA).

Techniques: Expressing