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nf κb inhibitor triptolide tpl (MedChemExpress)

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MedChemExpress nf κb inhibitor triptolide tpl

Knockdown of S100A4 inhibited <t>the</t> <t>NF-κB</t> signaling pathway and reduced the expression of NLRP3 inflammasome and pyroptosis-related proteins. ( A , B ) si- S100A4 downregulated the expression of p-NF-κB. The protein expression levels of p-NF-κB and NF-κB were analyzed using Western blot in the THP-1 macrophages pre-treated with si- S100A4 for 24 h and infected with BCG for 24 h subsequently. ( C – E ) The protein expression levels of p-NF-κB and NF-κB in the THP-1 macrophages, which were pre-treated with <t>Triptolide</t> <t>(TPL)</t> 5 nM for 2 h and infected with BCG for 24 h, were quantitatively analyzed using Western blot. ( F , G ) Inhibition of NF-κB decreased the expression of inflammatory-related proteins (NLRP3, Caspase-1 p48, ASC) and a pyroptosis-related protein (GSDMD-N). Data are from mean ± SD of three independent experiments, ns p > 0.05, * p < 0.05, *** p < 0.001.

Nf κb Inhibitor Triptolide Tpl, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 95/100, based on 93 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/triptolide/Triptolide/pmc10454862-151-0-7
Average 95 stars, based on 93 article reviews

nf κb inhibitor triptolide tpl - by Bioz Stars, 2026-11

95/100 stars

Images

1) Product Images from "S100A4 Promotes BCG-Induced Pyroptosis of Macrophages by Activating the NF-κB/NLRP3 Inflammasome Signaling Pathway"

Article Title: S100A4 Promotes BCG-Induced Pyroptosis of Macrophages by Activating the NF-κB/NLRP3 Inflammasome Signaling Pathway

Journal: International Journal of Molecular Sciences

doi: 10.3390/ijms241612709

Knockdown of S100A4 inhibited the NF-κB signaling pathway and reduced the expression of NLRP3 inflammasome and pyroptosis-related proteins. ( A , B ) si- S100A4 downregulated the expression of p-NF-κB. The protein expression levels of p-NF-κB and NF-κB were analyzed using Western blot in the THP-1 macrophages pre-treated with si- S100A4 for 24 h and infected with BCG for 24 h subsequently. ( C – E ) The protein expression levels of p-NF-κB and NF-κB in the THP-1 macrophages, which were pre-treated with Triptolide (TPL) 5 nM for 2 h and infected with BCG for 24 h, were quantitatively analyzed using Western blot. ( F , G ) Inhibition of NF-κB decreased the expression of inflammatory-related proteins (NLRP3, Caspase-1 p48, ASC) and a pyroptosis-related protein (GSDMD-N). Data are from mean ± SD of three independent experiments, ns p > 0.05, * p < 0.05, *** p < 0.001.

Figure Legend Snippet: Knockdown of S100A4 inhibited the NF-κB signaling pathway and reduced the expression of NLRP3 inflammasome and pyroptosis-related proteins. ( A , B ) si- S100A4 downregulated the expression of p-NF-κB. The protein expression levels of p-NF-κB and NF-κB were analyzed using Western blot in the THP-1 macrophages pre-treated with si- S100A4 for 24 h and infected with BCG for 24 h subsequently. ( C – E ) The protein expression levels of p-NF-κB and NF-κB in the THP-1 macrophages, which were pre-treated with Triptolide (TPL) 5 nM for 2 h and infected with BCG for 24 h, were quantitatively analyzed using Western blot. ( F , G ) Inhibition of NF-κB decreased the expression of inflammatory-related proteins (NLRP3, Caspase-1 p48, ASC) and a pyroptosis-related protein (GSDMD-N). Data are from mean ± SD of three independent experiments, ns p > 0.05, * p < 0.05, *** p < 0.001.

Techniques Used: Knockdown, Expressing, Western Blot, Infection, Inhibition

S100A4 activates the NF-κB/NLRP3 inflammasome signaling pathway to promote pyroptosis. THP-1 macrophages were pre-treated with MCC950 and TPL for 2 h, followed by the addition of exogenous S100A4 , and then infected with BCG for 24 h. ( A – F ) Western blot was used to detect the protein expression of ( B ) GSDMD-N, ( C ) p-NF-κB, ( D ) NLRP3, ( E ) Caspase-1, and ( F ) ASC. Data are from mean ± SD of three independent experiments, ns p > 0.05, * p < 0.05, ** p < 0.01, *** p < 0.001.

Figure Legend Snippet: S100A4 activates the NF-κB/NLRP3 inflammasome signaling pathway to promote pyroptosis. THP-1 macrophages were pre-treated with MCC950 and TPL for 2 h, followed by the addition of exogenous S100A4 , and then infected with BCG for 24 h. ( A – F ) Western blot was used to detect the protein expression of ( B ) GSDMD-N, ( C ) p-NF-κB, ( D ) NLRP3, ( E ) Caspase-1, and ( F ) ASC. Data are from mean ± SD of three independent experiments, ns p > 0.05, * p < 0.05, ** p < 0.01, *** p < 0.001.

Techniques Used: Infection, Western Blot, Expressing

Schematic diagram of S100A4 promoting BCG-induced pyroptosis in THP-1 macrophages through activation of the NF-κB/NLRP3 inflammasome signaling pathway.

Figure Legend Snippet: Schematic diagram of S100A4 promoting BCG-induced pyroptosis in THP-1 macrophages through activation of the NF-κB/NLRP3 inflammasome signaling pathway.

Techniques Used: Activation Assay

Concentration Assay:

Article Title: Transcription condensates are promoter hubs that enhance transcriptional bursts
Article Snippet: .. We prepared a 1000x stock concentration of triptolide (TPL, MedChemExpress, HY-32735) and (+)-JQ-1 (MedChemExpress, HY-13030), respectively in DMSO. ..

Article Title: Multi-cohort transcriptomics and donor-aware single-cell analyses prioritize S100A8 within an emergency-myeloid, HLA-DR-low state in sepsis
Article Snippet: .. Triptolide (MedChemExpress, HY-32735) was prepared as a DMSO stock and diluted immediately before use; all treatment groups had the same final DMSO concentration. .. Lipopolysaccharide from Escherichia coli O55:B5 (Sigma-Aldrich, 93572-42-0) was used.

other:

Article Title: Integrating multi-omics approaches reveals metabolic reprogramming and identifies PDHX as a candidate node in triptolide-treated non-small Cell lung cancer
Article Snippet: Triptolide (10 mM in DMSO) was purchased from MedChemExpress.

Inhibition:

Article Title: Histone H4 acetyl-methyllysine marks accessible chromatin that resists compaction
Article Snippet: .. For transcriptional inhibition studies, HEK293T cells were treated with 10 μM triptolide (MCE, HY-32735) or 500 nM flavopiridol (Sigma Aldrich, F3055) for 1hr. .. Unless otherwise indicated in the figure captions, experiments targeting KDM6A/B were performed by treating HEK293T cells with 5 μM GSK-J4 (MCE, HY-15648B) for either 6 or 24 hrs.

Solubility:

Article Title: Deep-learning-enabled morphodynamic analysis of drug responses in a biomimetic fibrin-based 3D glioblastoma invasion model
Article Snippet: .. The drugs tested in this study were: temozolomide (TMZ), dinaciclib, ixazomib, triptolide, and napabucasin (MedChemExpress, Princeton, NJ).These drugs were dissolved in dimethyl sulfoxide (DMSO) (Sigma-Aldrich, St. Louis, MO) at stock concentrations 100 mM (TMZ, dinaciclib, and ixazomib), 80 mM (triptolide), and 20mM (napabucasin), based on their maximal solubility, and stored at -80oC in the dark. ..

Image Search Results

(A) L1000CDS2 candidate screen highlighting 16-hydroxytriptolide. (B) Structures of triptolide and 16-hydroxytriptolide. (C,D) Representative triptolide docking pose and interface contacts in the S100A8 homodimer (PDB 5HLO). (E) Matched score differences between compounds across A/C and B/D receptors and Vina/Vinardo scoring. Scores from different functions are not directly comparable. (F) Contact-set Jaccard indices. (G) Complex and apo backbone RMSD across three 100-ns replicates. (H) Triptolide displacement from the original pocket, showing retention in replicate 2 and migration in replicates 1 and 3. Docking and dynamics do not establish direct binding.

Journal: PLOS One

Article Title: Multi-cohort transcriptomics and donor-aware single-cell analyses prioritize S100A8 within an emergency-myeloid, HLA-DR-low state in sepsis

doi: 10.1371/journal.pone.0359578

Figure Lengend Snippet: (A) L1000CDS2 candidate screen highlighting 16-hydroxytriptolide. (B) Structures of triptolide and 16-hydroxytriptolide. (C,D) Representative triptolide docking pose and interface contacts in the S100A8 homodimer (PDB 5HLO). (E) Matched score differences between compounds across A/C and B/D receptors and Vina/Vinardo scoring. Scores from different functions are not directly comparable. (F) Contact-set Jaccard indices. (G) Complex and apo backbone RMSD across three 100-ns replicates. (H) Triptolide displacement from the original pocket, showing retention in replicate 2 and migration in replicates 1 and 3. Docking and dynamics do not establish direct binding.

Article Snippet: Triptolide (MedChemExpress, HY-32735) was prepared as a DMSO stock and diluted immediately before use; all treatment groups had the same final DMSO concentration.

Techniques: Docking Assay, Migration, Binding Assay

(A) Eight-condition siNC/siS100A8×Control/TPL/LPS/LPS + TPL immunoblots. (B,C) p-NF-κB/total NF-κB and S100A8/β-actin across three independent experiments. (D) Four-condition siRNA × LPS immunoblots. (E-G) CD74/β-actin, HLA-DRα/β-actin, and S100A8/β-actin. (H) TPL effects under LPS and the dependency contrast. The p-NF-κB dependency contrast was −0.011 (95% CI −0.249 to 0.226; P = 0.857); the three-way interaction was P = 0.848.

Journal: PLOS One

Article Title: Multi-cohort transcriptomics and donor-aware single-cell analyses prioritize S100A8 within an emergency-myeloid, HLA-DR-low state in sepsis

doi: 10.1371/journal.pone.0359578

Figure Lengend Snippet: (A) Eight-condition siNC/siS100A8×Control/TPL/LPS/LPS + TPL immunoblots. (B,C) p-NF-κB/total NF-κB and S100A8/β-actin across three independent experiments. (D) Four-condition siRNA × LPS immunoblots. (E-G) CD74/β-actin, HLA-DRα/β-actin, and S100A8/β-actin. (H) TPL effects under LPS and the dependency contrast. The p-NF-κB dependency contrast was −0.011 (95% CI −0.249 to 0.226; P = 0.857); the three-way interaction was P = 0.848.

Article Snippet: Triptolide (MedChemExpress, HY-32735) was prepared as a DMSO stock and diluted immediately before use; all treatment groups had the same final DMSO concentration.

Techniques: Western Blot

Triptolide promotes the clearance of intracellular SA and MRSA. (A) Schematic diagram of the procedure for screening TCM monomers that modulate intracellular SA clearance. (B) Representative results illustrating the effects of 15 TCM monomers that promoted intracellular SA clearance and 2 that inhibited it. DMSO and methicillin were used as the negative and positive controls, respectively. Intracellular survival analysis of SA (C) and MRSA (D) in iBMDMs treated with different concentrations of the designated TCM monomers. Data are shown as mean ± SEM [n = 3 in (B–D) ]. ***0.0001 ≤ P < 0.001; **** P < 0.0001 [one-way ANOVA with Dunnett’s post hoc test for (B–D) ].

Journal: Frontiers in Pharmacology

Article Title: Triptolide clears Staphylococcus aureus infection by targeting XIAP to induce host apoptosis while maintaining gut microbiota homeostasis

doi: 10.3389/fphar.2026.1834558

Figure Lengend Snippet: Triptolide promotes the clearance of intracellular SA and MRSA. (A) Schematic diagram of the procedure for screening TCM monomers that modulate intracellular SA clearance. (B) Representative results illustrating the effects of 15 TCM monomers that promoted intracellular SA clearance and 2 that inhibited it. DMSO and methicillin were used as the negative and positive controls, respectively. Intracellular survival analysis of SA (C) and MRSA (D) in iBMDMs treated with different concentrations of the designated TCM monomers. Data are shown as mean ± SEM [n = 3 in (B–D) ]. ***0.0001 ≤ P < 0.001; **** P < 0.0001 [one-way ANOVA with Dunnett’s post hoc test for (B–D) ].

Article Snippet: For transcriptomics analysis, total RNA was extracted from iBMDMs infected with SA and treated with DMSO or triptolide, and from lung macrophages of mice infected with SA or MRSA treated with PBS, triptolide, or methicillin according to the TRIzol® manual (Life Technologies, 15596-026).

Techniques:

Triptolide triggers activation of the apoptotic signaling pathway. Gene Ontology (GO) enrichment analysis of differentially expressed genes (A) and proteins (B) in SA-infected iBMDMs treated with triptolide versus DMSO. Volcano maps depicting differentially expressed genes (C) and proteins (D) in SA-infected iBMDMs treated with triptolide versus DMSO. (E) Representative results of fluorescence-activated cell sorting (FACS)-based analysis for percentages of apoptotic cells. Quantification of apoptosis in SA (F) - and MRSA (G) -infected cells treated with DMSO, triptolide, or methicillin. Immunoblotting analysis of cleaved caspase-3 in SA (H) - and MRSA (I) -infected cells treated with DMSO, triptolide, or methicillin. Q-VD-OPh was used as the caspase inhibitor. Data are shown as mean ± SEM [n = 4 in (F,G) ]. **** P < 0.0001 [two-way ANOVA with Tukey’s post-hoc test for (F,G) ].

Journal: Frontiers in Pharmacology

Article Title: Triptolide clears Staphylococcus aureus infection by targeting XIAP to induce host apoptosis while maintaining gut microbiota homeostasis

doi: 10.3389/fphar.2026.1834558

Figure Lengend Snippet: Triptolide triggers activation of the apoptotic signaling pathway. Gene Ontology (GO) enrichment analysis of differentially expressed genes (A) and proteins (B) in SA-infected iBMDMs treated with triptolide versus DMSO. Volcano maps depicting differentially expressed genes (C) and proteins (D) in SA-infected iBMDMs treated with triptolide versus DMSO. (E) Representative results of fluorescence-activated cell sorting (FACS)-based analysis for percentages of apoptotic cells. Quantification of apoptosis in SA (F) - and MRSA (G) -infected cells treated with DMSO, triptolide, or methicillin. Immunoblotting analysis of cleaved caspase-3 in SA (H) - and MRSA (I) -infected cells treated with DMSO, triptolide, or methicillin. Q-VD-OPh was used as the caspase inhibitor. Data are shown as mean ± SEM [n = 4 in (F,G) ]. **** P < 0.0001 [two-way ANOVA with Tukey’s post-hoc test for (F,G) ].

Techniques: Activation Assay, Infection, Fluorescence, FACS, Western Blot

Triptolide induces apoptosis through targeting XIAP. (A) Measurement of triptolide binding affinity to Bcl2, STAT1, and XIAP by octet. (B) Molecular docking analysis between triptolide and XIAP. The BIR2 and BIR3 domains of XIAP are shown in orange. RMSD (C) and Rg (D) curves depicting the interaction between triptolide and XIAP. RMSD, root mean square deviation; Rg, radius of gyration. (E) Blocking assay to assess the effect of triptolide or SM-164 on XIAP-caspase-3/9 interaction. Quantification of apoptosis in SA (F) - and MRSA (G) -infected cells treated with DMSO, triptolide, SM-164, triptolide in combination with SM-164, or methicillin. Data are shown as mean ± SEM [n = 3 in (F,G) ]. **0.001 ≤ P < 0.01; ***0.0001 ≤ P < 0.001; **** P < 0.0001 [one-way ANOVA with Dunnett’s post hoc test for (F,G) ].

Journal: Frontiers in Pharmacology

Article Title: Triptolide clears Staphylococcus aureus infection by targeting XIAP to induce host apoptosis while maintaining gut microbiota homeostasis

doi: 10.3389/fphar.2026.1834558

Figure Lengend Snippet: Triptolide induces apoptosis through targeting XIAP. (A) Measurement of triptolide binding affinity to Bcl2, STAT1, and XIAP by octet. (B) Molecular docking analysis between triptolide and XIAP. The BIR2 and BIR3 domains of XIAP are shown in orange. RMSD (C) and Rg (D) curves depicting the interaction between triptolide and XIAP. RMSD, root mean square deviation; Rg, radius of gyration. (E) Blocking assay to assess the effect of triptolide or SM-164 on XIAP-caspase-3/9 interaction. Quantification of apoptosis in SA (F) - and MRSA (G) -infected cells treated with DMSO, triptolide, SM-164, triptolide in combination with SM-164, or methicillin. Data are shown as mean ± SEM [n = 3 in (F,G) ]. **0.001 ≤ P < 0.01; ***0.0001 ≤ P < 0.001; **** P < 0.0001 [one-way ANOVA with Dunnett’s post hoc test for (F,G) ].

Techniques: Binding Assay, Blocking Assay, Infection

Triptolide reduces SA and MRSA survival and attenuates host inflammatory pathology in vivo (A) Diagram of the experimental design in mice. Bacterial loads of SA (B) and MRSA (C) in the lungs of C57BL/6N mice treated with PBS, triptolide, or methicillin. (D) Representative images and quantitation for inflammatory areas in the lungs of C57BL/6N mice treated as in (B,C) . Scale bar, 100 μm. (E) Immunofluorescence and quantitation for cleaved caspase-3 (red) in the lung macrophages (green) of C57BL/6N mice treated as in (B,C) . Scale bar, 20 μm. Data are shown as mean ± SEM [n = 4 in (B–E) ]. *0.01 ≤ P < 0.5; **0.001 ≤ P < 0.01; ***0.0001 ≤ P < 0.001; **** P < 0.0001 [one-way ANOVA with Tukey’s post-hoc test for (B–E) ].

Journal: Frontiers in Pharmacology

Article Title: Triptolide clears Staphylococcus aureus infection by targeting XIAP to induce host apoptosis while maintaining gut microbiota homeostasis

doi: 10.3389/fphar.2026.1834558

Figure Lengend Snippet: Triptolide reduces SA and MRSA survival and attenuates host inflammatory pathology in vivo (A) Diagram of the experimental design in mice. Bacterial loads of SA (B) and MRSA (C) in the lungs of C57BL/6N mice treated with PBS, triptolide, or methicillin. (D) Representative images and quantitation for inflammatory areas in the lungs of C57BL/6N mice treated as in (B,C) . Scale bar, 100 μm. (E) Immunofluorescence and quantitation for cleaved caspase-3 (red) in the lung macrophages (green) of C57BL/6N mice treated as in (B,C) . Scale bar, 20 μm. Data are shown as mean ± SEM [n = 4 in (B–E) ]. *0.01 ≤ P < 0.5; **0.001 ≤ P < 0.01; ***0.0001 ≤ P < 0.001; **** P < 0.0001 [one-way ANOVA with Tukey’s post-hoc test for (B–E) ].

Techniques: In Vivo, Quantitation Assay, Immunofluorescence

Transcriptomics and proteomics analysis revealing that triptolide induces apoptosis in lung macrophages from mice infected with SA or MRSA. (A) GO enrichment analysis of differentially expressed genes in SA-infected mice treated with PBS, triptolide, or methicillin. (B) GO enrichment analysis of differentially expressed genes in MRSA-infected mice treated with PBS, triptolide, or methicillin. (C) GO enrichment analysis of differentially expressed proteins in mice treated as in (A) . (D) GO enrichment analysis of differentially expressed proteins in mice treated as in (B) .

Journal: Frontiers in Pharmacology

Article Title: Triptolide clears Staphylococcus aureus infection by targeting XIAP to induce host apoptosis while maintaining gut microbiota homeostasis

doi: 10.3389/fphar.2026.1834558

Figure Lengend Snippet: Transcriptomics and proteomics analysis revealing that triptolide induces apoptosis in lung macrophages from mice infected with SA or MRSA. (A) GO enrichment analysis of differentially expressed genes in SA-infected mice treated with PBS, triptolide, or methicillin. (B) GO enrichment analysis of differentially expressed genes in MRSA-infected mice treated with PBS, triptolide, or methicillin. (C) GO enrichment analysis of differentially expressed proteins in mice treated as in (A) . (D) GO enrichment analysis of differentially expressed proteins in mice treated as in (B) .

Techniques: Transcriptomics, Infection

Metagenomics analysis revealing that triptolide maintains microbiota homeostasis in mice infected with SA or MRSA. (A) Alpha (α) diversity among SA-infected mice treated with PBS, triptolide, or methicillin. (B) Alpha (α) diversity among MRSA-infected mice treated with PBS, triptolide, or methicillin. (C) Differential analysis of gut microbial composition among SA-infected mice treated as in (A) . (D) Differential analysis of gut microbial composition among MRSA-infected mice treated as in (B) .

Journal: Frontiers in Pharmacology

Article Title: Triptolide clears Staphylococcus aureus infection by targeting XIAP to induce host apoptosis while maintaining gut microbiota homeostasis

doi: 10.3389/fphar.2026.1834558

Figure Lengend Snippet: Metagenomics analysis revealing that triptolide maintains microbiota homeostasis in mice infected with SA or MRSA. (A) Alpha (α) diversity among SA-infected mice treated with PBS, triptolide, or methicillin. (B) Alpha (α) diversity among MRSA-infected mice treated with PBS, triptolide, or methicillin. (C) Differential analysis of gut microbial composition among SA-infected mice treated as in (A) . (D) Differential analysis of gut microbial composition among MRSA-infected mice treated as in (B) .

Techniques: Metagenomics, Infection

Metabolomics analysis revealing that triptolide enhances immunomodulatory metabolites against infections. (A) Partial least-squares discriminant analysis (PLS-DA) score plots of metabolites from SA-infected mice treated with PBS, triptolide, or methicillin. (B) PLS-DA score plots of metabolites from MRSA-infected mice treated with PBS, triptolide, or methicillin. (C) Heatmap of differential metabolites among SA-infected mice treated as in (A) . (D) Heatmap of differential metabolites among MRSA-infected mice treated as in (B) .

Journal: Frontiers in Pharmacology

Article Title: Triptolide clears Staphylococcus aureus infection by targeting XIAP to induce host apoptosis while maintaining gut microbiota homeostasis

doi: 10.3389/fphar.2026.1834558

Figure Lengend Snippet: Metabolomics analysis revealing that triptolide enhances immunomodulatory metabolites against infections. (A) Partial least-squares discriminant analysis (PLS-DA) score plots of metabolites from SA-infected mice treated with PBS, triptolide, or methicillin. (B) PLS-DA score plots of metabolites from MRSA-infected mice treated with PBS, triptolide, or methicillin. (C) Heatmap of differential metabolites among SA-infected mice treated as in (A) . (D) Heatmap of differential metabolites among MRSA-infected mice treated as in (B) .

Techniques: Infection

Review

nf κb inhibitor triptolide tpl (MedChemExpress)

Structured Review

Images

1) Product Images from "S100A4 Promotes BCG-Induced Pyroptosis of Macrophages by Activating the NF-κB/NLRP3 Inflammasome Signaling Pathway"

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