Journal: Journal of Cosmetic Dermatology

Article Title: Naringenin as a Multifunctional Ingredient Targeting Pathways Associated With Skin Inflammaging: Preclinical and Clinical Evidence

doi: 10.1111/jocd.71167

Figure Lengend Snippet: Naringenin regulates the expression of multiple biological pathways, including many associated with inflammation. (A) Naringenin is not cytotoxic in the range of tested concentrations using a predefined cell viability threshold of > 80% relative to control. Data are presented as a mean +/− SD ( n = 3). All treatment groups showed no statistically significant differences compared to the untreated control (ns = not significant). (B) Example genes associated with inflammation that are downregulated by naringenin in keratinocytes. * p < 0.01. (C) Detailed map of the TNF signaling pathway (from the Kyoto Encyclopedia of Genes and Genomes) superimposed with the modulation of individual genes by naringenin. (D) A visual representation of Gene Set Enrichment Analysis emphasizing the biological processes affected by naringenin. NES = Normalized Enrichment Score.

Article Snippet: Levels of TNF‐α and IL‐6 were quantified using commercially available ELISA kits (ELH‐TNFa, ELH‐IL6‐1, RayBiotech, Peachtree Corners, GA, USA) according to the manufacturer's instructions.

Techniques: Expressing, Control

Journal: Journal of Cosmetic Dermatology

Article Title: Naringenin as a Multifunctional Ingredient Targeting Pathways Associated With Skin Inflammaging: Preclinical and Clinical Evidence

doi: 10.1111/jocd.71167

Figure Lengend Snippet: Naringenin has anti‐inflammatory activity, as shown by reductions in the inflammation markers IL‐6 (A) and TNF‐α (B). An asterisk (*) indicates the test product concentrations (% w/w ) that showed statistically significant differences compared to stimulated controls. Unstimulated and stimulated controls are colored gray, naringenin treatments orange, and niacinamide benchmark comparison charcoal. Data are plotted as mean +/− SD, with a statistically significant threshold of p < 0.05.

Article Snippet: Levels of TNF‐α and IL‐6 were quantified using commercially available ELISA kits (ELH‐TNFa, ELH‐IL6‐1, RayBiotech, Peachtree Corners, GA, USA) according to the manufacturer's instructions.

Techniques: Activity Assay, Comparison

Journal: Cell Reports Medicine

Article Title: A biomimetic hybrid membrane vesicle nanoplatform attenuates tendinopathy through neuroinflammation modulation and tendon regeneration

doi: 10.1016/j.xcrm.2026.102937

Figure Lengend Snippet: MSM-DTM adsorbs inflammatory cytokines, suppresses TSPCs inflammation and senescence, and promotes tenogenic differentiation and migration (A) The remaining concentrations of TNF-α, IL-1β, IL-6, IFN-γ, LPS, and NGF were detected by ELISA after co-culture with different concentrations of MSM. (B and C) RT-qPCR of IL-6 and CCL-2 in TSPCs under different treatments. (D) Western blot of COL1A2, MMP3, and TNMD. (E) ELISA of TNF-α, IL-6, and IFN-γ in supernatants. (F)Western blot of p16 and p21 after 7 days of treatment. (G) β-Galactosidase staining analysis after 7 days of treatment. Scale bars, 100 μm. (H and I) Immunofluorescence and quantification of TNMD and TNC after 14-day treatment. Scale bars, 50 μm. (J) Relative mRNA expression of tenogenic differentiation markers SCX and TNC. (K and L) Representative images and quantification of Transwell assay. Scale bars, 100 μm. (M and N) Representative images and quantification of wound healing assay. Scale bars, 100 μm. Statistical comparisons were performed with one-way ANOVA with Tukey’s multiple comparisons test. Data are presented as the mean ± SD, n = 3. Ns, no significance, ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001 between groups.

Article Snippet: TNF-α ELISA kit , ABclonal , RK00030.

Techniques: Migration, Enzyme-linked Immunosorbent Assay, Co-Culture Assay, Quantitative RT-PCR, Western Blot, Staining, Immunofluorescence, Expressing, Transwell Assay, Wound Healing Assay

Journal: Cell Reports Medicine

Article Title: A biomimetic hybrid membrane vesicle nanoplatform attenuates tendinopathy through neuroinflammation modulation and tendon regeneration

doi: 10.1016/j.xcrm.2026.102937

Figure Lengend Snippet:

Article Snippet: TNF-α ELISA kit , ABclonal , RK00030.

Techniques: Recombinant, Lysis, Hydroxyproline Assay, Enzyme-linked Immunosorbent Assay, Isolation, SYBR Green Assay, Bicinchoninic Acid Protein Assay, Staining, Software

Journal: bioRxiv

Article Title: FluoroFate: A generalisable platform for time-resolved single-cell analysis of cell fate enables quantification of cell death dynamics

doi: 10.64898/2026.08.17.745187

Figure Lengend Snippet: ( A ) Schematic overview of TNFα/TNFR1 signalling. Engagement of TNFR1 promotes formation of membrane-associated complex I, leading to activation of NF-κB and MAPK signalling pathways and induction of pro-survival gene expression. Disruption of this pathway can result in formation of cytosolic complex IIa, leading to caspase activation and apoptosis. Birinapant promotes degradation of cIAP1/2, destabilising complex I and favouring early complex II formation, whereas cycloheximide inhibits protein synthesis and prevents accumulation of pro-survival factors downstream of TNFR1 signalling. ( B ) Quantification of live cells following treatment with TNFα, birinapant, or their combination (BT), assessed by flow cytometry in MDA-MB-231 cells. Cells were stained with Annexin V and propidium iodide (PI), and live cells were defined as Annexin V-negative/PI-negative. Data represent mean ± SD from three independent biological replicates. ( C ) Time-resolved analysis of cell viability following treatment with TNFα in combination with birinapant ( left ) or cycloheximide ( right ). Live-cell percentages were quantified from IncuCyte live-cell imaging using FluoroFate. BT treatment induces rapid and near-complete loss of viability, whereas CT treatment results in delayed but progressive cell death, demonstrating distinct temporal dynamics depending on the mode of TNFα pathway perturbation. ( D ) Representative live-cell imaging of MDA-MB-231 cells over the first 6 hours following treatment with untreated control (UT), BT, or CT. Annexin V-positive cells (green) and PI-positive cells (red) are shown overlaid on brightfield images. BT treatment results in rapid and widespread Annexin V staining, whereas CT treatment shows delayed onset of cell death. Scale bar, 100 μm. [ E ] Flow cytometry analysis of Annexin V staining over the first 6 hours following BT treatment. Representative dot plots show progressive increase in Annexin V-positive cells over time, confirming rapid induction of apoptosis at the single-cell level. Statistical significance was determined using one-way ANOVA with Dunnett’s post-hoc test, with **** indicating P < 0.0001 and ns indicating non-significant differences.

Article Snippet: Recombinant human tumour necrosis factor alpha (TNFα) was obtained from RayBiotech, birinapant from Apexbio, cycloheximide from Cell Signaling Technology, Annexin V-FITC from Biotium, and propidium iodide from Abcam.

Techniques: Membrane, Activation Assay, Gene Expression, Disruption, Flow Cytometry, Staining, Live Cell Imaging, Control, Single Cell

Journal: bioRxiv

Article Title: FluoroFate: A generalisable platform for time-resolved single-cell analysis of cell fate enables quantification of cell death dynamics

doi: 10.64898/2026.08.17.745187

Figure Lengend Snippet: ( A ) Schematic overview of TNFα/TNFR1 signalling, illustrating that disruption of complex IIa can promote formation of cytosolic complex IIb, from which signalling through RIPK1/RIPK3/MLKL can drive non-apoptotic cell death. ( B ) Western blot analysis of apoptotic signalling following BT treatment in MDA-MB-231 cells over the indicated time course. Cleavage of PARP, caspase 3, and caspase 8 confirms induction of apoptosis. Autophosphorylation of RIPK1 (p-RIPK1) at Ser166 and reduction of cIAP1 levels demonstrate modulation of TNFα/TNFR1 signalling. Β-actin serves as a loading control. ( C ) FluoroFate analysis of cell death dynamics in MDA-MB-231 cells following treatment with BT ( left ) or CT ( right ). The proportion of cells undergoing apoptosis (Annexin V-positive prior to PI), non-apoptotic cell death (PI-positive prior to or concurrent with Annexin V), and total cell death is shown. BT induces rapid and predominantly apoptotic cell death, whereas CT results in delayed and more heterogeneous cell death dynamics. ( D ) Quantification of live cells in SKOV3 WT and RIPK1 KO cells following BT treatment, assessed by flow cytometry. Cells were stained with Annexin V-FITC and PI, and live cells were defined as Annexin V-negative/PI-negative. RIPK1 KO cells exhibit increased resistance to BT-induced cell death compared to WT cells. [ E ] FluoroFate analysis of cell viability in SKOV3 WT and RIPK1 KO cells following BT treatment. Loss of RIPK1 delays and reduces overall cell death kinetics. ( F ) Single-cell classification of apoptotic and non-apoptotic cell death in SKOV3 WT ( left ) and RIPK1 KO ( right ) cells following BT treatment. Loss of RIPK1 selectively reduces apoptotic cell death, whilst non-apoptotic cell death remains largely unchanged, indicating that distinct modes of cell death are independently regulated at the single-cell level. Data represent mean ± SD from three biological replicates. Statistical significance was determined using two-way ANOVA followed by Fisher’s LSD post-hoc test (***P ≤ 0.0002, ****P < 0.0001, ns, not significant).

Article Snippet: Recombinant human tumour necrosis factor alpha (TNFα) was obtained from RayBiotech, birinapant from Apexbio, cycloheximide from Cell Signaling Technology, Annexin V-FITC from Biotium, and propidium iodide from Abcam.

Techniques: Disruption, Western Blot, Control, Flow Cytometry, Staining, Single Cell

Journal: Advanced Science

Article Title: Senkyunolide I Inhibits mtDNA‐cGAS‐STING Signaling in Macrophages via Targeting VDAC1 Oligomerization to Attenuate Ulcerative Colitis

doi: 10.1002/advs.77045

Figure Lengend Snippet: SEI inhibits DSS‐induced colonic inflammation and suppresses M1 polarization of macrophages. (A) qRT‐PCR analysis of inflammatory cytokines ( IL‐1β , IL‐6 , TNF‐α and IL‐23 ) ( n = 6). (B) ELISA for inflammatory cytokine production in colonic tissue, including IL‐1β, IL‐6, TNF‐α and IL‐23 ( n = 6). (C) The protein expression of iNOS and CD86 in colonic tissue was determined by WB ( n = 6). (D) Representative immunofluorescence images of colonic tissue stained for F4/80 (red) and CD86 (green) with DAPI (blue) for nuclear counterstaining. Scale bar = 50 µm. (E) Relative fluorescence intensity of CD86 + F4/80 + cells was quantified ( n = 4). (F) Flow cytometry gating strategy. (G) Representative flow cytometry dot plot. SEI reduced the levels of CD86 + M1‐type macrophages in the colonic lamina propria and increased the levels of F4/80 + CD206 + M2‐type macrophages. Bars are color‐coded to represent experimental groups: light blue = H 2 O‐treated normal control; red = DSS‐induced acute UC model; pale blue = 5‐ASA‐treated positive control (co‐administered with DSS); dark blue = low‐dose SEI (12.5 mg/kg) + DSS; purple = medium‐dose SEI (25 mg/kg) + DSS; green = high‐dose SEI (50 mg/kg) + DSS. Values were expressed as mean ± SD. # p < 0.05, ### p < 0.001 versus H 2 O group; * p < 0.05, ** p < 0.01, *** p < 0.001 versus DSS group.

Article Snippet: Senkyunolide I (HY‐N0745), Erastin (HY‐15763), H‐151 (HY‐112693), TNF‐α (HY‐P7058 or HY‐P7090), IFN‐γ (HY‐P7025 or HY‐P7071), Lipopolysaccharides (LPS, HY‐D1056), Adenosine 5'‐triphosphate (ATP, HY‐B2176) were purchased from MedChem Express.

Techniques: Quantitative RT-PCR, Enzyme-linked Immunosorbent Assay, Expressing, Immunofluorescence, Staining, Fluorescence, Flow Cytometry, Control, Positive Control

Journal: Advanced Science

Article Title: Senkyunolide I Inhibits mtDNA‐cGAS‐STING Signaling in Macrophages via Targeting VDAC1 Oligomerization to Attenuate Ulcerative Colitis

doi: 10.1002/advs.77045

Figure Lengend Snippet: ABPP proteomic analysis confirms VDAC1 as target protein of SEI. (A) Chemical structures of SEI and SEI probe (SEI‐P). (B) Cell viability of iBMDM cells treated with SEI or SEI‐P. (C) Release of inflammatory cytokine IL‐1β and (D) cell viability in TNF‐α plus IFN‐γ‐induced iBMDM cells. (E) Cellular imaging of SEI‐P with different exposure times in iBMDM cells. (F) Dose‐dependent labeling of proteins by SEI‐P in iBMDM cells. (G) Competition between SEI and SEI‐P for protein binding in situ (red star: 35 kD). (H) Chemical proteomics analysis workflow for identifying potential targets of SEI, created using Figdraw. (I) Volcano plot of proteins identified in the ABPP method. The graph displayed the log 2 FC of the competition group (100 µ m SEI + 50 µ m SEI‐P) versus SEI‐P (50 µ m ) ( x ‐axis) against the −log 10 ( p‐ value) ( y ‐axis). Among these, points with p < 0.05 and log 2 FC < −1 (blue) were selected as target protein candidates. Values were expressed as mean ± SD ( n = 3).

Article Snippet: Senkyunolide I (HY‐N0745), Erastin (HY‐15763), H‐151 (HY‐112693), TNF‐α (HY‐P7058 or HY‐P7090), IFN‐γ (HY‐P7025 or HY‐P7071), Lipopolysaccharides (LPS, HY‐D1056), Adenosine 5'‐triphosphate (ATP, HY‐B2176) were purchased from MedChem Express.

Techniques: Imaging, Labeling, Protein Binding, In Situ

Journal: Advanced Science

Article Title: Senkyunolide I Inhibits mtDNA‐cGAS‐STING Signaling in Macrophages via Targeting VDAC1 Oligomerization to Attenuate Ulcerative Colitis

doi: 10.1002/advs.77045

Figure Lengend Snippet: SEI directly interacts with VDAC1 to inhibit its oligomerization. (A) The interaction between SEI and VDAC1 was detected using molecular docking. (B) Lysates from iBMDM cells were incubated with or without SEI (100 µ m ) for 24 h. Different concentrations of pronase E were added for 20 min, and VDAC1 content was analyzed using WB analysis. (C) Lysates from iBMDM cells were incubated with SEI at the indicated concentrations for 24 h, with a final concentration of 0.01% pronase E added for 20 min. The level of VDAC1 was assessed through WB analysis. (D) iBMDM cells were incubated with SEI (100 µ m ) for 24 h. These samples were then analyzed using CETSA. Values were expressed as mean ± SD ( n = 3). * p < 0.05, ** p < 0.01 versus SEI group. (E) MST demonstrating a direct interaction between SEI and EGFP‐tagged VDAC1 in lysates from EGFP‐VDAC1 expressing HEK293T cells. (F) Immunoblotting analysis of VDAC1 cross‐linking in iBMDM cells, untreated or stimulated with TNF‐α plus IFN‐γ, with or without addition of SEI (100 µ m ). (G) The VDAC1‐OE plasmid was transfected into iBMDM cells, and cGAMP production was subsequently measured by ELISA. (H) iBMDM cells were transfected with VDAC1‐OE, and then the phosphorylation levels of STING and IRF3 were measured by WB. (I) The mRNA expression levels of CCL5 , CXCL10 , and ISG15 in iBMDM cells transfected with VDAC1‐OE were measured by qRT‐PCR. (J) qRT‐PCR analysis of cytoplasmic mtDNA ( mt‐Nd1 , D‐loop and mt‐Cytb ). Values were expressed as mean ± SD ( n = 3). * p < 0.05, ** p < 0.01, *** p < 0.001.

Article Snippet: Senkyunolide I (HY‐N0745), Erastin (HY‐15763), H‐151 (HY‐112693), TNF‐α (HY‐P7058 or HY‐P7090), IFN‐γ (HY‐P7025 or HY‐P7071), Lipopolysaccharides (LPS, HY‐D1056), Adenosine 5'‐triphosphate (ATP, HY‐B2176) were purchased from MedChem Express.

Techniques: Incubation, Concentration Assay, Expressing, Western Blot, Plasmid Preparation, Transfection, Enzyme-linked Immunosorbent Assay, Phospho-proteomics, Quantitative RT-PCR

Journal: Advanced Science

Article Title: Senkyunolide I Inhibits mtDNA‐cGAS‐STING Signaling in Macrophages via Targeting VDAC1 Oligomerization to Attenuate Ulcerative Colitis

doi: 10.1002/advs.77045

Figure Lengend Snippet: SEI directly binds to K12 on VDAC1. (A) The RMSD of the VDAC1 backbone was simulated for a range of 100 ns. (B) The RMSF values of all amino acid residues were simulated. (C) Radius of gyration of the apo (blue) and protein when bound to the ligand (red) for the 100 ns simulation. (D) DCCM analysis matrix of VDAC1 protein; the region in red indicates residue pairs in horizontal and vertical coordinates have positive correlation in movement patterns, while the region in blue indicates negative correlation. (E) DCCM analysis matrix of SEI‐VDAC1 complex. (F–H) Movement correlation of each residue with a negative correlation coefficient ranged from −0.6 to −0.8 of VDAC1 protein (F), ranged from −0.4 to −0.6 of VDAC1 protein (G), and ranged from −0.4 to −0.6 of SEI‐VDAC1 complex (H). (I) The total binding free energy was calculated, and a series of contribution components were analyzed. Data are presented as energy changes in units of kJ/mol. (J) Ten residues of the VDAC1‐SEI complex were selected and analyzed. Data were presented as energy changes in a unit of kJ/mol with different contributors indicated by colors. (K) Free energy landscape. (L) Sequence conservation analysis of VDAC1 protein using ESPript 3.0. (M) The iBMDM cells were transfected with K174, K12, and G172 mutation plasmids and then treated with DMSO or SEI (100 µ m ) for 1 h. The interaction between SEI and VDAC1 was detected using the CETSA assay. Values were expressed as mean ± SD ( n = 3). * p < 0.05, ** p < 0.01, *** p < 0.001 versus Ctrl group. (N) VDAC1 −/− iBMDM cells were transfected with Flag‐VDAC1(WT), Flag‐VDAC1(K174A), Flag‐VDAC1(K12A), or Flag‐VDAC1(G172A). Immunoblotting analysis of VDAC1 cross‐linking in iBMDM cells stimulated with TNF‐α plus IFN‐γ, with or without addition of SEI (100 µ m ). (O) VDAC1 −/− iBMDM cells were transfected with an empty vector, Flag‐VDAC1‐WT, Flag‐VDAC1(K174A), Flag‐VDAC1(K12A), or Flag‐VDAC1(G172A). WB analyses of the quantity of p‐TBK1 and p‐IRF3 after stimulation with TNF‐α plus IFN‐γ and treatment with SEI (100 µ m ) or left untreated (control) for 24 h. Values were expressed as mean ± SD ( n = 3). * p < 0.05, ** p < 0.01, *** p < 0.001.

Article Snippet: Senkyunolide I (HY‐N0745), Erastin (HY‐15763), H‐151 (HY‐112693), TNF‐α (HY‐P7058 or HY‐P7090), IFN‐γ (HY‐P7025 or HY‐P7071), Lipopolysaccharides (LPS, HY‐D1056), Adenosine 5'‐triphosphate (ATP, HY‐B2176) were purchased from MedChem Express.

Techniques: Residue, Binding Assay, Sequencing, Transfection, Mutagenesis, Western Blot, Plasmid Preparation, Control

Journal: Advanced Science

Article Title: Senkyunolide I Inhibits mtDNA‐cGAS‐STING Signaling in Macrophages via Targeting VDAC1 Oligomerization to Attenuate Ulcerative Colitis

doi: 10.1002/advs.77045

Figure Lengend Snippet: The VDAC1 K12 site is required for the protective roles of SEI in UC mice. (A) Daily assessments of body weight change and (B) DAI were conducted ( n = 6). (C) Gross morphology images of the colon were captured on day 9 after DSS treatment, and (D) colon length was measured ( n = 6). (E) The spleen index of mice after DSS treatment. (F) Colonic sections from mice were subjected to H&E staining ( U ‐shaped curve: U ‐shaped crypt; arrow: goblet cell; circle: inflammatory cells), and (G) a semiquantitative histological score was assessed ( n = 6). (H) Representative fluorescent images of MUC2, ZO1, Claudin1 and Occludin in the colonic tissues ( n = 4). (I) Representative fluorescent images of TFF3 in the colonic tissues ( n = 4). (J) IF staining for Ki67 and E‐cadherin in colon tissues ( n = 4). (K) ELISA for inflammatory cytokine production in colonic tissues, including IL‐1β, IL‐6, TNF‐α, and IL‐23 ( n = 6). (L) IF staining for F4/80 (red) and CD86 (green) in colon tissues ( n = 4). Scale bar = 50 µm. Values were expressed as mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001.

Article Snippet: Senkyunolide I (HY‐N0745), Erastin (HY‐15763), H‐151 (HY‐112693), TNF‐α (HY‐P7058 or HY‐P7090), IFN‐γ (HY‐P7025 or HY‐P7071), Lipopolysaccharides (LPS, HY‐D1056), Adenosine 5'‐triphosphate (ATP, HY‐B2176) were purchased from MedChem Express.

Techniques: Staining, Enzyme-linked Immunosorbent Assay

Journal: Nutrition Research and Practice

Article Title: Isothiocyanates inhibit the cisplatin-induced apoptosis and inflammation in human kidney HEK-293 cells

doi: 10.4162/nrp.2026.20.4.709

Figure Lengend Snippet: (A, B) Intracellular ROS accumulation was detected using the DCFDA assay. Intracellular ROS levels were estimated using a fluorescence plate reader at Ex/Em = 485/535 nm. (C, D) HEK-293 cells were treated with AITC and BITC for 24 h and subsequently exposed to cisplatin for 24 h before harvest. To estimate the NO concentration, the culture supernatant was assayed using the Griess reagent. HEK-293 cells were treated with AITC and BITC for 24 h and subsequently exposed to cisplatin for 24 h before harvest. (E-H) An ELISA kit was employed to measure IL-6 and TNF-α secretion. (I, J) TNF-α and COX-2 expression levels were measured using immunoblotting, and (K-N) densities were normalized to β-actin using ImageJ software. Cells were harvested, and (O-R) TNF-α and COX-2 mRNA expression levels in cisplatin-induced HEK-293 cells were evaluated. Experiments were performed at least in triplicate, and the results are presented as the mean ± SD. Different letters indicate significant differences ( P < 0.05), as determined using Duncan’s multiple-range test. CP, cisplatin; AITC, allyl isothiocyanate; BITC, benzyl isothiocyanate; TNF-α, tumor necrosis factor-α; IL-6, interleukin-6; COX-2, cyclooxygenase-2; HEK-293 cells, human embryonic kidney-293 cells; ELISA, enzyme-linked immunosorbent assay.

Article Snippet: To determine the effect of ITCs on cytokine production in cisplatin-treated HEK-293 cells, Cell-free supernatants were collected, and cytokine levels were measured using IL-6 and TNF-α ELISA kits (Raybiotech, Norcross, GA, USA).

Techniques: Fluorescence, Concentration Assay, Enzyme-linked Immunosorbent Assay, Expressing, Western Blot, Software

Journal: Nutrition Research and Practice

Article Title: Isothiocyanates inhibit the cisplatin-induced apoptosis and inflammation in human kidney HEK-293 cells

doi: 10.4162/nrp.2026.20.4.709

Figure Lengend Snippet: NF-κB protein levels were measured using (A, B) immunoblotting, and (C, D) densities were normalized to β-actin using ImageJ software. Cells were harvested, and (E, F) NF-κB mRNA expression in cisplatin-induced HEK-293 cells was evaluated. Data are presented as the mean ± SD. Different letters indicate significant differences ( P < 0.05), as determined using Duncan’s multiple-range test. (G, H) HEK-293 cells were treated with AITC and BITC and fixed with 4% paraformaldehyde. After blocking with an appropriate buffer, cells were incubated with antibodies. Thereafter, DAPI staining was performed to confirm cell nuclei. Signals were quantified using fluorescence microscopy at 400× magnification. CP, cisplatin; AITC, allyl isothiocyanate; BITC, benzyl isothiocyanate; TNF-α, tumor necrosis factor-α; IL-6, interleukin-6; COX-2, cyclooxygenase-2; HEK-293 cells, human embryonic kidney-293 cells; NF-κB, nuclear factor-κB; DAPI, 4′,6-diamidino-2-phenylindole.

Article Snippet: To determine the effect of ITCs on cytokine production in cisplatin-treated HEK-293 cells, Cell-free supernatants were collected, and cytokine levels were measured using IL-6 and TNF-α ELISA kits (Raybiotech, Norcross, GA, USA).

Techniques: Western Blot, Software, Expressing, Blocking Assay, Incubation, Staining, Fluorescence, Microscopy