anti nf κ b  (Servicebio Inc)

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 membranes were blocked with 5% milk for 1 h and then incubated with the following primary antibodies at 4 °C overnight: mouse anti-NLRP3 (1:1,000, Adipogen, AG-20B-0014), rabbit anti-BECN1 (1:1,000; Abcam, ab62557), rabbit anti-ASC (1:1,000, Adipogen, AG-25B-0006), mouse anti-RTN4 (1:1,000; BD, 612,238), mouse anti-caspase-1 (1:1,000, Adipogen, AG-20B-0042), rabbit anti-NF- κ B p65 (1:1,000, Cell Signaling Technology, 8,242), rabbit anti- p-NF- κ B p65 (1:1,000, Cell Signaling Technology, 3,033), rabbit anti-TNF-α (1:2,000, Abcam, ab6671), rabbit anti-IL-1β (1:2,000, GeneTex, GTX74034), rabbit anti-ICAM-1 (1:2,000, Immunoway, YM8074), mouse anti-GAPDH (1:10,000, Proteintech Group, 60004-I-Ig) and rabbit anti-VCAM-1 (1:4,000, Abcam, ab134047).

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 membranes were blocked with 5% milk for 1 h and then incubated with the following primary antibodies at 4 °C overnight: mouse anti-NLRP3 (1:1,000, Adipogen, AG-20B-0014), rabbit anti-BECN1 (1:1,000; Abcam, ab62557), rabbit anti-ASC (1:1,000, Adipogen, AG-25B-0006), mouse anti-RTN4 (1:1,000; BD, 612,238), mouse anti-caspase-1 (1:1,000, Adipogen, AG-20B-0042), rabbit anti-NF- κ B p65 (1:1,000, Cell Signaling Technology, 8,242), rabbit anti- p-NF- κ B p65 (1:1,000, Cell Signaling Technology, 3,033), rabbit anti-TNF-α (1:2,000, Abcam, ab6671), rabbit anti-IL-1β (1:2,000, GeneTex, GTX74034), rabbit anti-ICAM-1 (1:2,000, Immunoway, YM8074), mouse anti-GAPDH (1:10,000, Proteintech Group, 60004-I-Ig) and rabbit anti-VCAM-1 (1:4,000, Abcam, ab134047).

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 membranes were blocked with 5% milk for 1 h and then incubated with the following primary antibodies at 4 °C overnight: mouse anti-NLRP3 (1:1,000, Adipogen, AG-20B-0014), rabbit anti-BECN1 (1:1,000; Abcam, ab62557), rabbit anti-ASC (1:1,000, Adipogen, AG-25B-0006), mouse anti-RTN4 (1:1,000; BD, 612,238), mouse anti-caspase-1 (1:1,000, Adipogen, AG-20B-0042), rabbit anti-NF- κ B p65 (1:1,000, Cell Signaling Technology, 8,242), rabbit anti- p-NF- κ B p65 (1:1,000, Cell Signaling Technology, 3,033), rabbit anti-TNF-α (1:2,000, Abcam, ab6671), rabbit anti-IL-1β (1:2,000, GeneTex, GTX74034), rabbit anti-ICAM-1 (1:2,000, Immunoway, YM8074), mouse anti-GAPDH (1:10,000, Proteintech Group, 60004-I-Ig) and rabbit anti-VCAM-1 (1:4,000, Abcam, ab134047).

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 membranes were blocked with 5% milk for 1 h and then incubated with the following primary antibodies at 4 °C overnight: mouse anti-NLRP3 (1:1,000, Adipogen, AG-20B-0014), rabbit anti-BECN1 (1:1,000; Abcam, ab62557), rabbit anti-ASC (1:1,000, Adipogen, AG-25B-0006), mouse anti-RTN4 (1:1,000; BD, 612,238), mouse anti-caspase-1 (1:1,000, Adipogen, AG-20B-0042), rabbit anti-NF- κ B p65 (1:1,000, Cell Signaling Technology, 8,242), rabbit anti- p-NF- κ B p65 (1:1,000, Cell Signaling Technology, 3,033), rabbit anti-TNF-α (1:2,000, Abcam, ab6671), rabbit anti-IL-1β (1:2,000, GeneTex, GTX74034), rabbit anti-ICAM-1 (1:2,000, Immunoway, YM8074), mouse anti-GAPDH (1:10,000, Proteintech Group, 60004-I-Ig) and rabbit anti-VCAM-1 (1:4,000, Abcam, ab134047).

Techniques: Knockdown, Activation Assay, Injection, Virus, Fluorescence, Staining, 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: 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 membranes were blocked with 5% milk for 1 h and then incubated with the following primary antibodies at 4 °C overnight: mouse anti-NLRP3 (1:1,000, Adipogen, AG-20B-0014), rabbit anti-BECN1 (1:1,000; Abcam, ab62557), rabbit anti-ASC (1:1,000, Adipogen, AG-25B-0006), mouse anti-RTN4 (1:1,000; BD, 612,238), mouse anti-caspase-1 (1:1,000, Adipogen, AG-20B-0042), rabbit anti-NF- κ B p65 (1:1,000, Cell Signaling Technology, 8,242), rabbit anti- p-NF- κ B p65 (1:1,000, Cell Signaling Technology, 3,033), rabbit anti-TNF-α (1:2,000, Abcam, ab6671), rabbit anti-IL-1β (1:2,000, GeneTex, GTX74034), rabbit anti-ICAM-1 (1:2,000, Immunoway, YM8074), mouse anti-GAPDH (1:10,000, Proteintech Group, 60004-I-Ig) and rabbit anti-VCAM-1 (1:4,000, Abcam, ab134047).

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 membranes were blocked with 5% milk for 1 h and then incubated with the following primary antibodies at 4 °C overnight: mouse anti-NLRP3 (1:1,000, Adipogen, AG-20B-0014), rabbit anti-BECN1 (1:1,000; Abcam, ab62557), rabbit anti-ASC (1:1,000, Adipogen, AG-25B-0006), mouse anti-RTN4 (1:1,000; BD, 612,238), mouse anti-caspase-1 (1:1,000, Adipogen, AG-20B-0042), rabbit anti-NF- κ B p65 (1:1,000, Cell Signaling Technology, 8,242), rabbit anti- p-NF- κ B p65 (1:1,000, Cell Signaling Technology, 3,033), rabbit anti-TNF-α (1:2,000, Abcam, ab6671), rabbit anti-IL-1β (1:2,000, GeneTex, GTX74034), rabbit anti-ICAM-1 (1:2,000, Immunoway, YM8074), mouse anti-GAPDH (1:10,000, Proteintech Group, 60004-I-Ig) and rabbit anti-VCAM-1 (1:4,000, Abcam, ab134047).

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 membranes were blocked with 5% milk for 1 h and then incubated with the following primary antibodies at 4 °C overnight: mouse anti-NLRP3 (1:1,000, Adipogen, AG-20B-0014), rabbit anti-BECN1 (1:1,000; Abcam, ab62557), rabbit anti-ASC (1:1,000, Adipogen, AG-25B-0006), mouse anti-RTN4 (1:1,000; BD, 612,238), mouse anti-caspase-1 (1:1,000, Adipogen, AG-20B-0042), rabbit anti-NF- κ B p65 (1:1,000, Cell Signaling Technology, 8,242), rabbit anti- p-NF- κ B p65 (1:1,000, Cell Signaling Technology, 3,033), rabbit anti-TNF-α (1:2,000, Abcam, ab6671), rabbit anti-IL-1β (1:2,000, GeneTex, GTX74034), rabbit anti-ICAM-1 (1:2,000, Immunoway, YM8074), mouse anti-GAPDH (1:10,000, Proteintech Group, 60004-I-Ig) and rabbit anti-VCAM-1 (1:4,000, Abcam, ab134047).

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 membranes were blocked with 5% milk for 1 h and then incubated with the following primary antibodies at 4 °C overnight: mouse anti-NLRP3 (1:1,000, Adipogen, AG-20B-0014), rabbit anti-BECN1 (1:1,000; Abcam, ab62557), rabbit anti-ASC (1:1,000, Adipogen, AG-25B-0006), mouse anti-RTN4 (1:1,000; BD, 612,238), mouse anti-caspase-1 (1:1,000, Adipogen, AG-20B-0042), rabbit anti-NF- κ B p65 (1:1,000, Cell Signaling Technology, 8,242), rabbit anti- p-NF- κ B p65 (1:1,000, Cell Signaling Technology, 3,033), rabbit anti-TNF-α (1:2,000, Abcam, ab6671), rabbit anti-IL-1β (1:2,000, GeneTex, GTX74034), rabbit anti-ICAM-1 (1:2,000, Immunoway, YM8074), mouse anti-GAPDH (1:10,000, Proteintech Group, 60004-I-Ig) and rabbit anti-VCAM-1 (1:4,000, Abcam, ab134047).

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

Journal: Frontiers in Immunology

Article Title: Yinhua Gouteng decoction alleviates tic disorder symptoms by modulating neuro-inflammation in a rat model

doi: 10.3389/fimmu.2025.1680975

Figure Lengend Snippet: YHGTD suppresses TLR4/MyD88/NF- κ B pathway activation in the striatum and colon of IDPN-induced TD rats. (a) Representative western blot images of TLR4, MyD88, p-I κ B- α , I κ B- α and NF- κ B p65 protein in the striatum; (b-f) Quantification of TLR4 (b) , MyD88 (c) , p-I κ B- α (d) , I κ B- α (e) , NF- κ B p65 (f) protein expression in the striatum; (g) Representative Western blot images of TLR4, MyD88, p-I κ B- α , I κ B- α and NF- κ B p65 protein in the colon; (h-l) Quantification of TLR4 (h) , MyD88 (i) , p-I κ B- α (j) , I κ B- α (k) , NF- κ B p65 (l) protein expression in the colon. n = 3 per group. Compared with the control group, △△ P <0.01, △△△ P <0.001; Compared with the model group, * P <0.05, ** P <0.01, *** P <0.001.

Article Snippet: The NF- κ B p65 antibody was purchased from Cell Signaling Technology (CST, Cat# D14E12, Danvers, MA, USA), and the TLR4 antibody from Affinity Biosciences (Cat# AF7017, Cincinnati, OH, USA).

Techniques: Activation Assay, Western Blot, Expressing, Control

Journal: Acta Pharmaceutica Sinica. B

Article Title: Inhalable songorine-integrated lipid nanomedicine for targeted ARDS therapy via repairing endothelial barrier and inactivating NLRP3 inflammasome

doi: 10.1016/j.apsb.2025.10.048

Figure Lengend Snippet: Son-lipo inhibited the activation of NLRP3 inflammasome. (A) The immunohistochemistry staining and (B) statistical analysis of NLRP3 and CASPASE-1 proteins ( n = 3). Scale bar = 100 μm. (C, D) The Nlrp3 and Casp1 transcripts in lung tissues by RT-qPCR ( n = 3). Internal control, α -Tubulin. (E) The binding activity between Son and TLR4 protein was shown by an in silico molecular docking analysis. (F) The protein expressions of TLR4, P-P65, P65, NLRP3, PRO-CASPASE-1, and CASPASE-1 in the lung tissues by Western blot and (G‒J) their statistical analysis ( n = 3). (K) Expression levels of IL-1 β by ELISA ( n = 4). Data are represented as mean ± SD. ∗ P < 0.05 vs Control. # P < 0.05 vs Model. † P < 0.05.

Article Snippet: The primary antibodies used above were ZO-1 (1:5000, Proteintech), TLR4 (1:500, Santa Cruz, sc-293072, CA, USA), NLRP3 (1:1000, Adipogen), pro-caspase-1/caspase-1 (1:1000, Adipogen), p-NF- κ B p65 (1:500, Santa Cruz, sc-166748, CA, USA), and NF- κ B p65 (1:500, Santa Cruz, sc-8008, CA, USA).

Techniques: Activation Assay, Immunohistochemistry, Staining, Quantitative RT-PCR, Control, Binding Assay, Activity Assay, In Silico, Western Blot, Expressing, Enzyme-linked Immunosorbent Assay

Journal: Acta Pharmaceutica Sinica. B

Article Title: Inhalable songorine-integrated lipid nanomedicine for targeted ARDS therapy via repairing endothelial barrier and inactivating NLRP3 inflammasome

doi: 10.1016/j.apsb.2025.10.048

Figure Lengend Snippet: Son-lipo inhibited the activation of NLRP3 inflammasome. (A) The immunohistochemistry staining and (B) statistical analysis of NLRP3 and CASPASE-1 proteins ( n = 3). Scale bar = 100 μm. (C, D) The Nlrp3 and Casp1 transcripts in lung tissues by RT-qPCR ( n = 3). Internal control, α -Tubulin. (E) The binding activity between Son and TLR4 protein was shown by an in silico molecular docking analysis. (F) The protein expressions of TLR4, P-P65, P65, NLRP3, PRO-CASPASE-1, and CASPASE-1 in the lung tissues by Western blot and (G‒J) their statistical analysis ( n = 3). (K) Expression levels of IL-1 β by ELISA ( n = 4). Data are represented as mean ± SD. ∗ P < 0.05 vs Control. # P < 0.05 vs Model. † P < 0.05.

Article Snippet: The primary antibodies used above were ZO-1 (1:5000, Proteintech), TLR4 (1:500, Santa Cruz, sc-293072, CA, USA), NLRP3 (1:1000, Adipogen), pro-caspase-1/caspase-1 (1:1000, Adipogen), p-NF- κ B p65 (1:500, Santa Cruz, sc-166748, CA, USA), and NF- κ B p65 (1:500, Santa Cruz, sc-8008, CA, USA).

Techniques: Activation Assay, Immunohistochemistry, Staining, Quantitative RT-PCR, Control, Binding Assay, Activity Assay, In Silico, Western Blot, Expressing, Enzyme-linked Immunosorbent Assay