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Cedarlane nsc34 neurons
PTEN -siRNA nanoparticle transfection enables efficient gene silencing with minimal impact on neuron health (A) PTEN -siRNA nanoparticles (100 nM) demonstrated highly efficient knockdown of target PTEN mRNA in differentiated <t>NSC34</t> neurons, with peak knockdown on Day 3 for the delivered siRNA [t(2) = −4.840, p = 0.02007; one-tailed] with expression levels returning to baseline by Day 7 [t(2) = 0.05373, p = 0.5190; one-tailed]. RNA fold change and associated error was assessed using the 2 −ΔΔCt method and normalized to GAPDH as per (B) Treatment of neurons with PTEN- siRNA nanoparticles at 100 nM had a non-significant effect on the metabolic activity at 3 [t(2) = 0.6370, p = 0.5893, 95 % CI 74.4820<x <134.3874] and 7 days [t(2) = −3.390, p = 0.07708, 95 % CI -66.21<x<104.0] post-transfection. (C – F) Transfection of PTEN -siRNA nanoparticles does not affect neuronal morphology. Control and PTEN -siRNA nanoparticle treated neurons have a similar distribution, density, and morphology compared to control neurons (C, D). Higher magnification images showed that all neurons (control and treated) possessed a typical neuronal morphology with several neurites extending from each cell body (E, F). All cells were stained for F-actin (green = phalloidin) and nuclei (blue = DAPI). Scale Bar in (C, D): 100 μm; Scale Bar in (E, F): 50 μm. Significance code: ns = p > 0.1; • = p ≤ 0.1, ∗ = p ≤ 0.05, ∗∗ = p ≤ 0.01, ∗∗∗ = p ≤ 0.001, ∗∗∗∗ = p ≤ 0.0001.
Nsc34 Neurons, supplied by Cedarlane, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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MedChemExpress nsc23766
PTEN -siRNA nanoparticle transfection enables efficient gene silencing with minimal impact on neuron health (A) PTEN -siRNA nanoparticles (100 nM) demonstrated highly efficient knockdown of target PTEN mRNA in differentiated <t>NSC34</t> neurons, with peak knockdown on Day 3 for the delivered siRNA [t(2) = −4.840, p = 0.02007; one-tailed] with expression levels returning to baseline by Day 7 [t(2) = 0.05373, p = 0.5190; one-tailed]. RNA fold change and associated error was assessed using the 2 −ΔΔCt method and normalized to GAPDH as per (B) Treatment of neurons with PTEN- siRNA nanoparticles at 100 nM had a non-significant effect on the metabolic activity at 3 [t(2) = 0.6370, p = 0.5893, 95 % CI 74.4820<x <134.3874] and 7 days [t(2) = −3.390, p = 0.07708, 95 % CI -66.21<x<104.0] post-transfection. (C – F) Transfection of PTEN -siRNA nanoparticles does not affect neuronal morphology. Control and PTEN -siRNA nanoparticle treated neurons have a similar distribution, density, and morphology compared to control neurons (C, D). Higher magnification images showed that all neurons (control and treated) possessed a typical neuronal morphology with several neurites extending from each cell body (E, F). All cells were stained for F-actin (green = phalloidin) and nuclei (blue = DAPI). Scale Bar in (C, D): 100 μm; Scale Bar in (E, F): 50 μm. Significance code: ns = p > 0.1; • = p ≤ 0.1, ∗ = p ≤ 0.05, ∗∗ = p ≤ 0.01, ∗∗∗ = p ≤ 0.001, ∗∗∗∗ = p ≤ 0.0001.
Nsc23766, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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MedChemExpress nsc228155
PTEN -siRNA nanoparticle transfection enables efficient gene silencing with minimal impact on neuron health (A) PTEN -siRNA nanoparticles (100 nM) demonstrated highly efficient knockdown of target PTEN mRNA in differentiated <t>NSC34</t> neurons, with peak knockdown on Day 3 for the delivered siRNA [t(2) = −4.840, p = 0.02007; one-tailed] with expression levels returning to baseline by Day 7 [t(2) = 0.05373, p = 0.5190; one-tailed]. RNA fold change and associated error was assessed using the 2 −ΔΔCt method and normalized to GAPDH as per (B) Treatment of neurons with PTEN- siRNA nanoparticles at 100 nM had a non-significant effect on the metabolic activity at 3 [t(2) = 0.6370, p = 0.5893, 95 % CI 74.4820<x <134.3874] and 7 days [t(2) = −3.390, p = 0.07708, 95 % CI -66.21<x<104.0] post-transfection. (C – F) Transfection of PTEN -siRNA nanoparticles does not affect neuronal morphology. Control and PTEN -siRNA nanoparticle treated neurons have a similar distribution, density, and morphology compared to control neurons (C, D). Higher magnification images showed that all neurons (control and treated) possessed a typical neuronal morphology with several neurites extending from each cell body (E, F). All cells were stained for F-actin (green = phalloidin) and nuclei (blue = DAPI). Scale Bar in (C, D): 100 μm; Scale Bar in (E, F): 50 μm. Significance code: ns = p > 0.1; • = p ≤ 0.1, ∗ = p ≤ 0.05, ∗∗ = p ≤ 0.01, ∗∗∗ = p ≤ 0.001, ∗∗∗∗ = p ≤ 0.0001.
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MedChemExpress canonical ferroptosis inhibitor
PTEN -siRNA nanoparticle transfection enables efficient gene silencing with minimal impact on neuron health (A) PTEN -siRNA nanoparticles (100 nM) demonstrated highly efficient knockdown of target PTEN mRNA in differentiated <t>NSC34</t> neurons, with peak knockdown on Day 3 for the delivered siRNA [t(2) = −4.840, p = 0.02007; one-tailed] with expression levels returning to baseline by Day 7 [t(2) = 0.05373, p = 0.5190; one-tailed]. RNA fold change and associated error was assessed using the 2 −ΔΔCt method and normalized to GAPDH as per (B) Treatment of neurons with PTEN- siRNA nanoparticles at 100 nM had a non-significant effect on the metabolic activity at 3 [t(2) = 0.6370, p = 0.5893, 95 % CI 74.4820<x <134.3874] and 7 days [t(2) = −3.390, p = 0.07708, 95 % CI -66.21<x<104.0] post-transfection. (C – F) Transfection of PTEN -siRNA nanoparticles does not affect neuronal morphology. Control and PTEN -siRNA nanoparticle treated neurons have a similar distribution, density, and morphology compared to control neurons (C, D). Higher magnification images showed that all neurons (control and treated) possessed a typical neuronal morphology with several neurites extending from each cell body (E, F). All cells were stained for F-actin (green = phalloidin) and nuclei (blue = DAPI). Scale Bar in (C, D): 100 μm; Scale Bar in (E, F): 50 μm. Significance code: ns = p > 0.1; • = p ≤ 0.1, ∗ = p ≤ 0.05, ∗∗ = p ≤ 0.01, ∗∗∗ = p ≤ 0.001, ∗∗∗∗ = p ≤ 0.0001.
Canonical Ferroptosis Inhibitor, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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MedChemExpress stat 3 inhibitor s3i 201
Majoon Ushba ablates the <t>IL-17A-JAK-2/STAT-3</t> signaling axis. (A) Relative protein expression of JAK-2, p-JAK-2, STAT-3, and p-STAT3 in IL-17A stimulated HaCaT cells. (B) Immunofluorescence of p-STAT3 to assess nuclear translocation. (C) Colony formation assay was performed to assess the ability of the IL-17A/JAK-2-STAT-3 pathway to influence cell proliferation, magnification: 20X, Scale bar: 100μm. Data are expressed as the mean ± SEM of n = 3 independent biological replicates (separate experiments). Each dot represents a single biological replicate from one independent experiment. Mean difference and confidence intervals are shown in the Supplementary Table 1 . Statistical significance was determined by one-way ANOVA followed by Bonferroni’s post-hoc test: # ( p < 0.05), ## ( p < 0.01), and ### ( p < 0.001) versus untreated HaCaT keratinocytes; * ( p < 0.05), ** p < 0.01, and *** p < 0.001 versus IL-17A-stimulated psoriasis-like keratinocytes. Abbreviations: JAK-2, Janus kinase 2; STAT3, Signal transducer and activator of transcription 3; IL-17A, Interleukin 17 A.
Stat 3 Inhibitor S3i 201, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


PTEN -siRNA nanoparticle transfection enables efficient gene silencing with minimal impact on neuron health (A) PTEN -siRNA nanoparticles (100 nM) demonstrated highly efficient knockdown of target PTEN mRNA in differentiated NSC34 neurons, with peak knockdown on Day 3 for the delivered siRNA [t(2) = −4.840, p = 0.02007; one-tailed] with expression levels returning to baseline by Day 7 [t(2) = 0.05373, p = 0.5190; one-tailed]. RNA fold change and associated error was assessed using the 2 −ΔΔCt method and normalized to GAPDH as per (B) Treatment of neurons with PTEN- siRNA nanoparticles at 100 nM had a non-significant effect on the metabolic activity at 3 [t(2) = 0.6370, p = 0.5893, 95 % CI 74.4820<x <134.3874] and 7 days [t(2) = −3.390, p = 0.07708, 95 % CI -66.21<x<104.0] post-transfection. (C – F) Transfection of PTEN -siRNA nanoparticles does not affect neuronal morphology. Control and PTEN -siRNA nanoparticle treated neurons have a similar distribution, density, and morphology compared to control neurons (C, D). Higher magnification images showed that all neurons (control and treated) possessed a typical neuronal morphology with several neurites extending from each cell body (E, F). All cells were stained for F-actin (green = phalloidin) and nuclei (blue = DAPI). Scale Bar in (C, D): 100 μm; Scale Bar in (E, F): 50 μm. Significance code: ns = p > 0.1; • = p ≤ 0.1, ∗ = p ≤ 0.05, ∗∗ = p ≤ 0.01, ∗∗∗ = p ≤ 0.001, ∗∗∗∗ = p ≤ 0.0001.

Journal: Bioactive Materials

Article Title: Development of a PTEN -siRNA activated scaffold to promote axonal regrowth following spinal cord injury

doi: 10.1016/j.bioactmat.2026.01.022

Figure Lengend Snippet: PTEN -siRNA nanoparticle transfection enables efficient gene silencing with minimal impact on neuron health (A) PTEN -siRNA nanoparticles (100 nM) demonstrated highly efficient knockdown of target PTEN mRNA in differentiated NSC34 neurons, with peak knockdown on Day 3 for the delivered siRNA [t(2) = −4.840, p = 0.02007; one-tailed] with expression levels returning to baseline by Day 7 [t(2) = 0.05373, p = 0.5190; one-tailed]. RNA fold change and associated error was assessed using the 2 −ΔΔCt method and normalized to GAPDH as per (B) Treatment of neurons with PTEN- siRNA nanoparticles at 100 nM had a non-significant effect on the metabolic activity at 3 [t(2) = 0.6370, p = 0.5893, 95 % CI 74.4820 0.1; • = p ≤ 0.1, ∗ = p ≤ 0.05, ∗∗ = p ≤ 0.01, ∗∗∗ = p ≤ 0.001, ∗∗∗∗ = p ≤ 0.0001.

Article Snippet: NSC34 neuronal culture and transfections: NSC34 neurons (Cedarlane Cat No. CLU140), a hybrid cell line produced by the fusion of motor neuron enriched embryonic mouse spinal cord cells with mouse neuroblastoma cells, were cultured in growth medium Dulbecco's Modified Eagle Medium (DMEM; Sigma-Aldrich, Ireland) supplemented with 10 % fetal bovine serum (FBS; Labtech UK), 1 % (v/v) L-Glutamine (Sigma-Aldrich, Ireland), and 1 % (v/v) Penicillin- Streptomycin Solution (Sigma-Aldrich, Ireland) in a T-175 cell culture flask (37 °C, 5 % CO 2 ).

Techniques: Transfection, Knockdown, One-tailed Test, Expressing, Activity Assay, Control, Staining

Scaffold-mediated siRNA delivery does not affect the viability of neurons, results in prolonged downregulation of PTEN, and stimulates increased expression of BCL2 and GAP43 mRNA . (A) The metabolic activity of NSC34 neurons cultured on PTEN -siRNA activated scaffolds peaked by day 3 post-transfection [t(2) = 4.0599, p = 0.05565, 95 % CI 93.954<x<308.3], decreased by day 7 [t(2) = −15.068, p = 0.004375, 95 % CI 49.7157<x<72.05] and was similar to control levels by day 21 [t(2) = −0.1042, p = 0.9265, 95 % CI 83.23<x<116.0]. Metabolic activity normalization was performed relative to the untreated cells. (B) LDH assay revealed a consistent but small increase in cell stress over a span of 21 days. (C – D) Analysis of PTEN gene expression in scaffold transfected neurons over 21 days showed a significant decrease in expression levels [t(4) = −3.2927, p = 0.01507; one-tailed] 3 days after transfection that was then followed by a gradual return toward untreated control levels denoted by the blue regression line which approaches the red untreated control line after 21 days. (E – F) The change in BCL2 expression 3-, 7-, and 21-days post-transfection showed a significant initial elevation [t(4) = 2.092, p = 0.05227, one-tailed], followed by a gradual reduction converging toward untreated control levels. (G – H). Similarly, GAP43 expression was characterised by of an initial significant rise [t(4) = 2.1748, p = 0.04765, one-tailed] in levels that was followed by a decrease over the 21-day culture period. Significance code: ns = p > 0.1; • = p ≤ 0.1, ∗ = p ≤ 0.05, ∗∗ = p ≤ 0.01, ∗∗∗ = p ≤ 0.001, ∗∗∗∗ = p ≤ 0.0001.

Journal: Bioactive Materials

Article Title: Development of a PTEN -siRNA activated scaffold to promote axonal regrowth following spinal cord injury

doi: 10.1016/j.bioactmat.2026.01.022

Figure Lengend Snippet: Scaffold-mediated siRNA delivery does not affect the viability of neurons, results in prolonged downregulation of PTEN, and stimulates increased expression of BCL2 and GAP43 mRNA . (A) The metabolic activity of NSC34 neurons cultured on PTEN -siRNA activated scaffolds peaked by day 3 post-transfection [t(2) = 4.0599, p = 0.05565, 95 % CI 93.954 0.1; • = p ≤ 0.1, ∗ = p ≤ 0.05, ∗∗ = p ≤ 0.01, ∗∗∗ = p ≤ 0.001, ∗∗∗∗ = p ≤ 0.0001.

Article Snippet: NSC34 neuronal culture and transfections: NSC34 neurons (Cedarlane Cat No. CLU140), a hybrid cell line produced by the fusion of motor neuron enriched embryonic mouse spinal cord cells with mouse neuroblastoma cells, were cultured in growth medium Dulbecco's Modified Eagle Medium (DMEM; Sigma-Aldrich, Ireland) supplemented with 10 % fetal bovine serum (FBS; Labtech UK), 1 % (v/v) L-Glutamine (Sigma-Aldrich, Ireland), and 1 % (v/v) Penicillin- Streptomycin Solution (Sigma-Aldrich, Ireland) in a T-175 cell culture flask (37 °C, 5 % CO 2 ).

Techniques: Expressing, Activity Assay, Cell Culture, Transfection, Control, Lactate Dehydrogenase Assay, Gene Expression, One-tailed Test

Majoon Ushba ablates the IL-17A-JAK-2/STAT-3 signaling axis. (A) Relative protein expression of JAK-2, p-JAK-2, STAT-3, and p-STAT3 in IL-17A stimulated HaCaT cells. (B) Immunofluorescence of p-STAT3 to assess nuclear translocation. (C) Colony formation assay was performed to assess the ability of the IL-17A/JAK-2-STAT-3 pathway to influence cell proliferation, magnification: 20X, Scale bar: 100μm. Data are expressed as the mean ± SEM of n = 3 independent biological replicates (separate experiments). Each dot represents a single biological replicate from one independent experiment. Mean difference and confidence intervals are shown in the Supplementary Table 1 . Statistical significance was determined by one-way ANOVA followed by Bonferroni’s post-hoc test: # ( p < 0.05), ## ( p < 0.01), and ### ( p < 0.001) versus untreated HaCaT keratinocytes; * ( p < 0.05), ** p < 0.01, and *** p < 0.001 versus IL-17A-stimulated psoriasis-like keratinocytes. Abbreviations: JAK-2, Janus kinase 2; STAT3, Signal transducer and activator of transcription 3; IL-17A, Interleukin 17 A.

Journal: Pharmaceutical Biology

Article Title: Majoon Ushba alleviated IL-17A sensitized keratinocyte ferroptosis via JAK-2-STAT-3 signaling axis and reversed imiquimod induced psoriasiform inflammation

doi: 10.1080/13880209.2026.2654904

Figure Lengend Snippet: Majoon Ushba ablates the IL-17A-JAK-2/STAT-3 signaling axis. (A) Relative protein expression of JAK-2, p-JAK-2, STAT-3, and p-STAT3 in IL-17A stimulated HaCaT cells. (B) Immunofluorescence of p-STAT3 to assess nuclear translocation. (C) Colony formation assay was performed to assess the ability of the IL-17A/JAK-2-STAT-3 pathway to influence cell proliferation, magnification: 20X, Scale bar: 100μm. Data are expressed as the mean ± SEM of n = 3 independent biological replicates (separate experiments). Each dot represents a single biological replicate from one independent experiment. Mean difference and confidence intervals are shown in the Supplementary Table 1 . Statistical significance was determined by one-way ANOVA followed by Bonferroni’s post-hoc test: # ( p < 0.05), ## ( p < 0.01), and ### ( p < 0.001) versus untreated HaCaT keratinocytes; * ( p < 0.05), ** p < 0.01, and *** p < 0.001 versus IL-17A-stimulated psoriasis-like keratinocytes. Abbreviations: JAK-2, Janus kinase 2; STAT3, Signal transducer and activator of transcription 3; IL-17A, Interleukin 17 A.

Article Snippet: The STAT-3 inhibitor S3I-201 and canonical ferroptosis inhibitor (ferrostain-1) were purchased from MedChem Express (NJ, USA).

Techniques: Expressing, Immunofluorescence, Translocation Assay, Colony Assay

Pharmacological ablation of psoriasis pathogenic mediators by Majoon Ushba via attenuating JAK-2-STAT-3 signaling axis. (A–C) Relative gene expression of Cyr61, HMGB1, and VEGF was assessed using RT-PCR. (D–F) Relative protein expression was assessed using immunofluorescence, magnification: 20X, Scale bar: 100μm. Data are expressed as the mean ± SEM of n = 3 independent biological replicates (separate experiments). Each dot represents a single biological replicate from one independent experiment. Mean difference and confidence intervals are shown in the supplementary Table 1 . Statistical significance was determined by one-way ANOVA followed by Bonferroni’s post-hoc test: # ( p < 0.05), ## ( p < 0.01), and ### ( p < 0.001) versus untreated HaCaT keratinocytes; * ( p < 0.05), ** p < 0.01, and *** p < 0.001 versus IL-17A-stimulated psoriasis-like keratinocytes.

Journal: Pharmaceutical Biology

Article Title: Majoon Ushba alleviated IL-17A sensitized keratinocyte ferroptosis via JAK-2-STAT-3 signaling axis and reversed imiquimod induced psoriasiform inflammation

doi: 10.1080/13880209.2026.2654904

Figure Lengend Snippet: Pharmacological ablation of psoriasis pathogenic mediators by Majoon Ushba via attenuating JAK-2-STAT-3 signaling axis. (A–C) Relative gene expression of Cyr61, HMGB1, and VEGF was assessed using RT-PCR. (D–F) Relative protein expression was assessed using immunofluorescence, magnification: 20X, Scale bar: 100μm. Data are expressed as the mean ± SEM of n = 3 independent biological replicates (separate experiments). Each dot represents a single biological replicate from one independent experiment. Mean difference and confidence intervals are shown in the supplementary Table 1 . Statistical significance was determined by one-way ANOVA followed by Bonferroni’s post-hoc test: # ( p < 0.05), ## ( p < 0.01), and ### ( p < 0.001) versus untreated HaCaT keratinocytes; * ( p < 0.05), ** p < 0.01, and *** p < 0.001 versus IL-17A-stimulated psoriasis-like keratinocytes.

Article Snippet: The STAT-3 inhibitor S3I-201 and canonical ferroptosis inhibitor (ferrostain-1) were purchased from MedChem Express (NJ, USA).

Techniques: Gene Expression, Reverse Transcription Polymerase Chain Reaction, Expressing, Immunofluorescence

Majoon Ushba abrogated the JAK-2-STAT-3 signaling axis in an IMQ-induced psoriasis mice model. Skin tissue from mice in the respective experimental groups was obtained following euthanasia and used to isolate total protein and RNA. (A) Relative protein levels of JAK-2, p-JAK2, STAT-3, and p-STAT3 were assessed using western blotting. (B) Additionally, the protein levels of Ki67, a cell proliferation marker, and p-STAT3 were assessed using immunohistochemistry, magnification: 20X, Scale bar: 100μm. Total RNA was used to measure the relative mRNA levels of (C) Cyr61, (D) HMGB1, and (E) VEGF by RT-PCR. The values are expressed as the mean ± SEM of n = 6 animal per group. Each data point (n = 6 per group) represents the average of three technical replicates. Mean difference and confidence intervals are shown in the Supplementary Table 1 . Statistical significance was determined by one-way ANOVA followed by Bonferroni’s post-hoc test: #p < 0.05, ##p < 0.01 and ### p < 0.01 verses control mice. * p < 0.05, ** p < 0.01 and *** p < 0.01 verses IMQ-induced psoriasis mice. Abbreviations: Cyr61, cysteine-rich angiogenic inducer 61; HMGB, High mobility group box 1; VEGF, Vascular endothelial growth factor.

Journal: Pharmaceutical Biology

Article Title: Majoon Ushba alleviated IL-17A sensitized keratinocyte ferroptosis via JAK-2-STAT-3 signaling axis and reversed imiquimod induced psoriasiform inflammation

doi: 10.1080/13880209.2026.2654904

Figure Lengend Snippet: Majoon Ushba abrogated the JAK-2-STAT-3 signaling axis in an IMQ-induced psoriasis mice model. Skin tissue from mice in the respective experimental groups was obtained following euthanasia and used to isolate total protein and RNA. (A) Relative protein levels of JAK-2, p-JAK2, STAT-3, and p-STAT3 were assessed using western blotting. (B) Additionally, the protein levels of Ki67, a cell proliferation marker, and p-STAT3 were assessed using immunohistochemistry, magnification: 20X, Scale bar: 100μm. Total RNA was used to measure the relative mRNA levels of (C) Cyr61, (D) HMGB1, and (E) VEGF by RT-PCR. The values are expressed as the mean ± SEM of n = 6 animal per group. Each data point (n = 6 per group) represents the average of three technical replicates. Mean difference and confidence intervals are shown in the Supplementary Table 1 . Statistical significance was determined by one-way ANOVA followed by Bonferroni’s post-hoc test: #p < 0.05, ##p < 0.01 and ### p < 0.01 verses control mice. * p < 0.05, ** p < 0.01 and *** p < 0.01 verses IMQ-induced psoriasis mice. Abbreviations: Cyr61, cysteine-rich angiogenic inducer 61; HMGB, High mobility group box 1; VEGF, Vascular endothelial growth factor.

Article Snippet: The STAT-3 inhibitor S3I-201 and canonical ferroptosis inhibitor (ferrostain-1) were purchased from MedChem Express (NJ, USA).

Techniques: Western Blot, Marker, Immunohistochemistry, Reverse Transcription Polymerase Chain Reaction, Control

In-Silico molecular docking analysis revealed strong binding partners against IL-17RA and STAT-3. (A–C) The prospective phytoconstituents catechin, morin, and quercetin, docked against IL-17R, showed stable interactions. (D–F) The phytoconstituents, Catechin, Morin and Quercetin docked against STAT-3 showing stable interactions.

Journal: Pharmaceutical Biology

Article Title: Majoon Ushba alleviated IL-17A sensitized keratinocyte ferroptosis via JAK-2-STAT-3 signaling axis and reversed imiquimod induced psoriasiform inflammation

doi: 10.1080/13880209.2026.2654904

Figure Lengend Snippet: In-Silico molecular docking analysis revealed strong binding partners against IL-17RA and STAT-3. (A–C) The prospective phytoconstituents catechin, morin, and quercetin, docked against IL-17R, showed stable interactions. (D–F) The phytoconstituents, Catechin, Morin and Quercetin docked against STAT-3 showing stable interactions.

Article Snippet: The STAT-3 inhibitor S3I-201 and canonical ferroptosis inhibitor (ferrostain-1) were purchased from MedChem Express (NJ, USA).

Techniques: In Silico, Binding Assay