pyrrolidinedithiocarbamate ammonium pdtc  (MedChemExpress)

Journal: Journal of Inflammation Research

Article Title: Celastrol Mitigates Acute Pancreatitis Associated Inflammation by Modulating the IL-34/CSF-1R Axis and Suppressing NF-κB/ERK Signaling

doi: 10.2147/JIR.S572609

Figure Lengend Snippet: Celastrol attenuates pancreatic injury and inflammatory mediator release in experimental AP. ( A ) Representative H&E staining of pancreatic tissue from Sham, AP, and Celastrol+AP rats with corresponding histological injury scores (scale bar: 100 μm). ( B ) Serum amylase levels (n = 6 rats per group). ( C ) Serum IL-6 and TNF-α levels measured by ELISA (n = 6 rats per group). ( D ) Amylase activity in AR42J cell supernatants under Con (Control), AP (caerulein), and AP plus PD98059, PDTC, or celastrol treatment (n=3 independent experiments). ( E ) IL-6 and TNF-α levels in AR42J cell supernatants (n = 3 independent experiments). Data are presented as mean ± SD. Each dot represents an individual animal or independent experiment. Statistical analysis was performed using one-way ANOVA for data in ( B–E ) with Tukey’s post-hoc test, except for histological scores in ( A ), which were analyzed by Kruskal–Wallis test. *P < 0.05, **P < 0.01, ***P < 0.001 vs AP group.

Article Snippet: To induce acinar-like differentiation, cells were treated with dexamethasone (Solarbio, D8040) for 48 h. After differentiation, cells were stimulated with caerulein (100 nM; MCE, HY-A0190) for 24 h to establish an in vitro AP model. For pharmacological intervention studies, cells were pretreated with celastrol (2.0 μM), PD98059 (10 μM; MCE, HY-12028), or PDTC (60 μM; MCE, HY-18738) for 1 h prior to caerulein stimulation, without removing the inhibitors.

Techniques: Staining, Enzyme-linked Immunosorbent Assay, Activity Assay, Control

Journal: Journal of Inflammation Research

Article Title: Celastrol Mitigates Acute Pancreatitis Associated Inflammation by Modulating the IL-34/CSF-1R Axis and Suppressing NF-κB/ERK Signaling

doi: 10.2147/JIR.S572609

Figure Lengend Snippet: IL-34 expression is increased in experimental AP and reduced by celastrol treatment. ( A ) Western blot analysis of IL-34 in pancreatic tissue with densitometric quantification normalized to GAPDH (n = 3 independent biological replicates). ( B ) Serum IL-34 levels measured by ELISA (n = 6 rats per group). ( C ) Representative immunohistochemical staining of IL-34 in pancreatic sections with quantitative analysis (scale bar: 50 μm; n = 6 rats per group). ( D ) Western blot analysis of IL-34 in AR42J cells under Con, AP, and AP plus PD98059, PDTC, or celastrol treatment (n = 3 independent biological replicates). Data are presented as mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001 vs AP group.

Article Snippet: To induce acinar-like differentiation, cells were treated with dexamethasone (Solarbio, D8040) for 48 h. After differentiation, cells were stimulated with caerulein (100 nM; MCE, HY-A0190) for 24 h to establish an in vitro AP model. For pharmacological intervention studies, cells were pretreated with celastrol (2.0 μM), PD98059 (10 μM; MCE, HY-12028), or PDTC (60 μM; MCE, HY-18738) for 1 h prior to caerulein stimulation, without removing the inhibitors.

Techniques: Expressing, Western Blot, Enzyme-linked Immunosorbent Assay, Immunohistochemical staining, Staining

Journal: Journal of Inflammation Research

Article Title: Celastrol Mitigates Acute Pancreatitis Associated Inflammation by Modulating the IL-34/CSF-1R Axis and Suppressing NF-κB/ERK Signaling

doi: 10.2147/JIR.S572609

Figure Lengend Snippet: CSF-1R–associated ERK/NF-κB signaling is activated during AP and modulated by celastrol. ( A ) Representative double immunofluorescence staining of CSF-1R (red) and amylase (green) in pancreatic tissue with DAPI nuclear counterstaining (blue). Colocalization indicates spatial association under inflammatory conditions (scale bar: 20 μm). ( B ) Western blot analysis of CSF-1R, p-ERK1/2, and p-p65 in pancreatic tissue (n = 3 independent biological replicates). ( C and D ) Western blot analysis of CSF-1R, p-ERK1/2, and p-p65 in AR42J cells under Con, AP, and AP plus PD98059, PDTC, or celastrol treatment (n = 3 independent biological replicates). The two closely migrating bands detected for p-ERK correspond to the phosphorylated forms of ERK1 (44 kDa) and ERK2 (42 kDa). Data are presented as mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001 vs AP group.

Article Snippet: To induce acinar-like differentiation, cells were treated with dexamethasone (Solarbio, D8040) for 48 h. After differentiation, cells were stimulated with caerulein (100 nM; MCE, HY-A0190) for 24 h to establish an in vitro AP model. For pharmacological intervention studies, cells were pretreated with celastrol (2.0 μM), PD98059 (10 μM; MCE, HY-12028), or PDTC (60 μM; MCE, HY-18738) for 1 h prior to caerulein stimulation, without removing the inhibitors.

Techniques: Double Immunofluorescence Staining, Western Blot

Journal: iScience

Article Title: LAR1 promotes breast carcinogenesis by activating NF-κB signaling pathway through binding and enhancing APOC1 expression

doi: 10.1016/j.isci.2025.114386

Figure Lengend Snippet: LAR1 knockdown inhibited p65 nuclear translocation in BC cells (A) The protein expression of p -AKT (Ser473), AKT, p -IKK (Ser180/181), and IKK in MDA-MB-231 cells after LAR1 knockdown and overexpression. (B) The protein expression of p -IκBα (ser32/ser36), IκBα, p-p65 (Ser536), and p65 in MDA-MB-231 cells after LAR1 knockdown and overexpression. (C) Representative images of immunofluorescence staining for p65 in MDA-MB-231 cells after LAR1 knockdown and overexpression. Scale bars, 50 μm. (D) Quantitative analysis for the percentage of nuclear p65-positive cells in images of immunofluorescence staining ( n = 3). (E) Cell viability of MDA-MB-231 cells treated with PDTC (25 μmol/L) for 24 h was detected by CCK-8 assay. (F) Invasion of MDA-MB-231 cells treated with PDTC (25 μmol/L) for 24 h were visualized by Transwell assays ( n = 3). Scale bars, 100 μm. Data were presented as the mean ± SD, with statistical significance assessed using one-way ANOVA (for the left image of D, for E and 7F) or unpaired t test (for the right image of D). ∗∗ p < 0.01, the oeLAR1 group vs. the Vector group. # p < 0.05 and ## p < 0.01, the oeLAR1+PDTC group vs. the oeLAR1+Vehicle group.

Article Snippet: MDA-MB-231 cells were treated with the NF- κB inhibitor PDTC (25 μmol/L, Cat#A800469, Macklin Inc., Shanghai, China) for 24 h. For mRNA stability analysis, MDA-MB-231 cells were treated with 10 μg/mL actinomycin D (Cat#HY-17559, MCE, USA) for different periods of time (0, 1, 2, 3, or 4 h).

Techniques: Knockdown, Translocation Assay, Expressing, Over Expression, Immunofluorescence, Staining, CCK-8 Assay, Plasmid Preparation

Journal: Frontiers in Cardiovascular Medicine

Article Title: NF- κ B aggravates cardiac vascular endothelial injury by sustained activation of the NLRP3 inflammasome after ischemic stroke in rats

doi: 10.3389/fcvm.2026.1673693

Figure Lengend Snippet: Brain ischemia induces sustained activation and inflammation of ECs in the heart. (A) GO biological process enrichment bubble chart of cardiac vascular tissues from Sham and dMCAO 2 w rats. (B) KEGG pathway enrichment bubble chart in cardiac vascular of Sham and dMCAO 2 w rats. (C) Heatmap of the relative protein levels of target proteins in NF- κ B signaling pathway. (D) The mRNA levels of p105, VCAM-1, ICAM-1, IL-1β and TNF-α in each group. (E) Western blotting shows the expression of p-p65, p65 , VCAM-1, ICAM-1, IL-1β, and TNF-α in vessels of the heart in the Sham and dMCAO animals. (F–J) Quantitative analysis of p-p65, VCAM-1, ICAM-1, IL-1β, and TNF-α levels relative to GAPDH. Each bar represents the mean ± SD. * p < 0.05 vs. Sham group ( n = 4 in each group). Sham, sham operation; dMCAO, distal middle cerebral artery occlusion; VCAM-1, vascular cell adhesion molecule 1; ICAM-1, intercellular cell adhesion molecule-1; IL-1β, interleukin-1 beta; TNF-α, tumor necrosis factor-alpha; w, week.

Article Snippet: The NLRP3-selective inflammasome inhibitor MCC950 (MedChemExpress, HY-12815A), the NF- κ B p65 inhibitor PDTC (MedChemExpress, HY-18738), or the vehicle (normal saline, NS) was injected intraperitoneally 24 h before dMCAO.

Techniques: Activation Assay, Western Blot, Expressing

Journal: Frontiers in Cardiovascular Medicine

Article Title: NF- κ B aggravates cardiac vascular endothelial injury by sustained activation of the NLRP3 inflammasome after ischemic stroke in rats

doi: 10.3389/fcvm.2026.1673693

Figure Lengend Snippet: PDTC inhibits the activation of NF- κ B signaling pathway and alleviates the activation of cardiac vascular endothelial cells after dMCAO. (A) Western blotting shows the expression of p-p65 and p65 in vessels of the heart in the Sham and dMCAO rats injected with Veh or PDTC. (B,C) Quantitative analysis of p-p65 and p65 levels relative to GAPDH. Each bar represents the mean ± SD. * p < 0.05 vs. Sham group, # p < 0.05 vs. dMCAO 2 w + Veh group ( n = 4 in each group). (D) Western blotting shows the expression of NLRP3, ASC, and Casp-1 in vessels of the heart in the Sham and dMCAO rats injected with Veh or PDTC. (E–G) Quantitative analysis of NLRP3, ASC, and Casp-1 levels relative to GAPDH. Each bar represents the mean ± SD. * p < 0.05 vs. Sham group, # p < 0.05 vs. dMCAO 2 w + Veh group ( n = 4 in each group). (H) The mRNA levels of VCAM-1, ICAM-1, IL-1β, and TNF-α in each group. (I) Western blotting shows the expression of VCAM-1, ICAM-1, IL-1β, and TNF-α in vessels of the heart in the Sham and dMCAO rats injected with Veh or PDTC. (J–M) Quantitative analysis of VCAM-1, ICAM-1, IL-1β, and TNF-α levels relative to GAPDH. Each bar represents the mean ± SD. * p < 0.05 vs. Sham group, # p < 0.05 vs. dMCAO 2 w + Veh group ( n = 4 in each group). Sham, sham operation; dMCAO, distal middle cerebral artery occlusion; NLRP3, NOD-like receptor thermal protein domain associated protein 3; ASC, apoptosis-associated speck-like protein containing a CARD; Casp-1, caspase-1; Veh, Vehicle; RECA-1, rat endothelial cell antibody 1; VCAM-1, vascular cell adhesion molecule 1; ICAM-1, intercellular cell adhesion molecule-1; IL-1β, interleukin-1 beta; TNF-α, tumor necrosis factor-alpha; w, week.

Article Snippet: The NLRP3-selective inflammasome inhibitor MCC950 (MedChemExpress, HY-12815A), the NF- κ B p65 inhibitor PDTC (MedChemExpress, HY-18738), or the vehicle (normal saline, NS) was injected intraperitoneally 24 h before dMCAO.

Techniques: Activation Assay, Western Blot, Expressing, Injection

Journal: Frontiers in Cardiovascular Medicine

Article Title: NF- κ B aggravates cardiac vascular endothelial injury by sustained activation of the NLRP3 inflammasome after ischemic stroke in rats

doi: 10.3389/fcvm.2026.1673693

Figure Lengend Snippet: PDTC inhibits the activation of NF- κ B signaling pathway. (A) Representative photomicrographs show the co-localization of p-p65 (green) and RECA-1 (red) in heart in the Sham and dMCAO rats injected with Veh or PDTC. (B) The degree of overlap between p-p65 and RECA-1 fluorescence based on the Pearson correlation coefficient in each group. (C) Quantitative analysis of CD45 + cells in each group. Each bar represents the mean ± SD. * p < 0.05 vs. Sham group, # p < 0.05 vs. dMCAO 2 w + Veh group ( n = 6 in each group).

Article Snippet: The NLRP3-selective inflammasome inhibitor MCC950 (MedChemExpress, HY-12815A), the NF- κ B p65 inhibitor PDTC (MedChemExpress, HY-18738), or the vehicle (normal saline, NS) was injected intraperitoneally 24 h before dMCAO.

Techniques: Activation Assay, Injection, Fluorescence

Journal: Frontiers in Cardiovascular Medicine

Article Title: NF- κ B aggravates cardiac vascular endothelial injury by sustained activation of the NLRP3 inflammasome after ischemic stroke in rats

doi: 10.3389/fcvm.2026.1673693

Figure Lengend Snippet: Knockdown of p65 in vessels of the heart inhibits the activation of NF- κ B signaling pathway and the activation of vascular endothelial cells after dMCAO. (A) Design of experiments in which rats were injected with NF- κ B adeno-associated virus vectors in tail vein and subjected to either Sham or dMCAO. (B) Representative photomicrographs show the co-localization of GFP (green) and RECA-1 (red) in heart from dMCAO rats with AAV- shNF-κB injection. Scale bar: 25 μm. The degree of overlap between GFP and RECA-1 fluorescence based on the Pearson correlation coefficient in dMCAO 2 w rats. (C) Representative NeuN staining indicates the cortical infarction. Scale bar: 2 mm. (D) Quantitative analysis of the relative infarct volumes. Each bar represents the mean ± SD. * p < 0.05 vs. Sham group ( n = 6 in each group). (E) Western blotting shows the expression of p-p65 and p65 in vessels of the heart in the Sham and dMCAO rats injected with AAV-shCon or AAV- shNF-κB . (F,G) Quantitative analysis of p-p65 and p65 levels relative to GAPDH. Each bar represents the mean ± SD. * p < 0.05 vs. Sham group, # p < 0.05 vs. dMCAO 2 w + AAV-shCon group ( n = 4 in each group). (H) Western blotting shows the expression of NLRP3, ASC, Casp-1, VCAM-1, ICAM-1, IL-1β, and TNF-α in vessels of the heart in the Sham and dMCAO rats injected with AAV-shCon or AAV- shNF-κB . (I–O) Quantitative analysis of NLRP3, ASC, Casp-1, VCAM-1, ICAM-1, IL-1β, and TNF-α levels relative to GAPDH. Each bar represents the mean ± SD. * p < 0.05 vs. Sham group, # p < 0.05 vs. dMCAO 2 w + AAV-shCon group ( n = 4 in each group).Sham, sham operation; dMCAO, distal middle cerebral artery occlusion; GFP, green fluorescent protein; NLRP3, NOD-like receptor thermal protein domain associated protein 3; ASC, apoptosis-associated speck-like protein containing a CARD; Casp-1, caspase-1; Veh, Vehicle; RECA-1, rat endothelial cell antibody 1; VCAM-1, vascular cell adhesion molecule 1; ICAM-1, intercellular cell adhesion molecule-1; IL-1β, interleukin-1 beta; TNF-α, tumor necrosis factor-alpha; w, week.

Article Snippet: The NLRP3-selective inflammasome inhibitor MCC950 (MedChemExpress, HY-12815A), the NF- κ B p65 inhibitor PDTC (MedChemExpress, HY-18738), or the vehicle (normal saline, NS) was injected intraperitoneally 24 h before dMCAO.

Techniques: Knockdown, Activation Assay, Injection, Virus, Fluorescence, Staining, Western Blot, Expressing