protein kinase mapk  (Cell Signaling Technology Inc)

Journal: Scientific Reports

Article Title: Triptolide induces apoptosis of glioma cells by inhibiting NF-κB activation during oxidative stress

doi: 10.1038/s41598-024-80856-7

Figure Lengend Snippet: Network pharmacological analysis and molecular docking. ( A )Triptolide and Neuroglioma cross targets. ( B ) KEGG pathway enrichment analysis of 8 cross targets. ( C ) GO enrichment analysis of 8 cross targets. ( D ) Triptolide-Intersection target protein-Signal transduction pathway network diagram. The pink color represents Triptolide, the blue-purple color represents 8 Intersection target proteins, and the inverted triangle symbolizes the Signal transduction pathway. The font size of the nodes indicates their degree value, a larger font size signifies a higher degree value, indicating greater importance of the node in the network and its closer association with Triptolide. ( E ) Enhanced 3D and 2D visualizations of molecular docking interactions between TP and CD14, Bcl-2, PLAU, PTGS2. ( F ) p-NF-κB, JNK and p38-MAPK in U251 cells were detected by immunofluorescence. ( G ) Quantitative analysis of p-NF-κB, JNK and p38-MAPK expression levels. (** P < 0.01) (Scale bar: 20 μm) ( n = 3).

Article Snippet: The cells were then incubated with primary antibodies against BCL2-Associated X (Bax), B-cell lymphoma-2 (Bcl-2), p-nuclear factor kappa-B (p-NF-κB), c-Jun N-terminal kinase (JNK), p38 mitogen-activated protein kinase (p38-MAPK), tumor necrosis factor-α (TNF-α), and interleukin-10 (IL-10) at 4℃ for 24 h. Next, the cells were incubated with a fluorescent secondary antibody (1:1000) (Thermo, Shanghai, China) for 1 h. The nuclei were then stained with 4’,6-diamidino-2-phenylindole (DAPI) for 5 min, and fluorescence images were obtained by fluorescence scanning microscopy (MIDI:3Dhistech, Panoramic, Hungary) for analysis using Image J.

Techniques: Transduction, Immunofluorescence, Expressing

Journal: Foods

Article Title: Role and Mechanism of Sialic Acid in Alleviating Acute Lung Injury through In Vivo and In Vitro Models

doi: 10.3390/foods13182984

Figure Lengend Snippet: Effects of SA supplementation on the JNK/p38/PPAR-γ-NF-κB pathway and the expressions of the oxidation-related genes of the lung tissues. The protein expressions of JNK, p38, NF-κB, and PPAR-γ were tested by western blot analysis ( A , B ). Effects of SA supplementation on the protein levels of oxidation-related genes (HO-1 and NQO1) ( C , D ). CON: control; LPS: lipopolysaccharide; LPS + 50 SA: LPS + 50 mg/kg/day SA; LPS + 100 SA: LPS + 100 mg/kg/day SA; SA: sialic acid. The data are expressed as mean ± SD. CON group vs. LPS group or LPS group vs. LPS + 50 SA group and LPS + 100 SA group. * p < 0.05. ** p < 0.01. # p > 0.05.

Article Snippet: Polyclonal antibody tumor necrosis factor-α (TNF-α, CAT. #6945S), interleukin-6 (IL-6, CAT. #12912S), interleukin-1β (IL-1β, CAT. #12242S), nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) p65 (CAT. #12629S), activator protein 1 (AP-1, CAT. #9165S), and mitogen-activated protein kinase (MAPK) family antibody (JNK, CAT. #9252S; p-JNK, CAT. #4668S; p38, CAT. #9212S; p-p38, CAT. #4511S) were provided by Cell Signaling Technology (Danver, MA, USA).

Techniques: Western Blot, Control

Journal: Foods

Article Title: Role and Mechanism of Sialic Acid in Alleviating Acute Lung Injury through In Vivo and In Vitro Models

doi: 10.3390/foods13182984

Figure Lengend Snippet: Effects of SA supplementation on the p38/JNK and Nrf2 pathways in LPS-induced HUVEC cells. HUVEC cells were pretreated with different dosages of SA (25, 50, and 100 μg/mL) for 2 h and then treated with LPS for 10–12 h. The total protein was obtained from the cells, and the protein expressions of p38, p-p38, JNK, and p-JNK were determined by western blot analysis ( A , B ). The effects of SA supplementation on the Nrf2 pathway ( C , D ). LPS: lipopolysaccharide; SA: sialic acid. Data are presented as the mean ± SD of three independent experiments. CON group vs. LPS group or LPS group vs. 25, 50, and 100 μg/mL SA group. * p < 0.05, ** p < 0.01. # p > 0.05.

Article Snippet: Polyclonal antibody tumor necrosis factor-α (TNF-α, CAT. #6945S), interleukin-6 (IL-6, CAT. #12912S), interleukin-1β (IL-1β, CAT. #12242S), nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) p65 (CAT. #12629S), activator protein 1 (AP-1, CAT. #9165S), and mitogen-activated protein kinase (MAPK) family antibody (JNK, CAT. #9252S; p-JNK, CAT. #4668S; p38, CAT. #9212S; p-p38, CAT. #4511S) were provided by Cell Signaling Technology (Danver, MA, USA).

Techniques: Western Blot

Journal: Foods

Article Title: Role and Mechanism of Sialic Acid in Alleviating Acute Lung Injury through In Vivo and In Vitro Models

doi: 10.3390/foods13182984

Figure Lengend Snippet: Schematic representation of the protective effect and possible molecular mechanisms of SA on ALI. SA exerted a protective effect against LPS-induced ALI via ameliorating inflammation and oxidative damage, which worked mainly through regulation of the JNK/p38-NF-κB/AP-1 and Nrf2 signaling pathways. ALI: acute lung injury; HUVEC: human umbilical vein endothelial cells; LPS: lipopolysaccharide; SA: sialic acid.

Article Snippet: Polyclonal antibody tumor necrosis factor-α (TNF-α, CAT. #6945S), interleukin-6 (IL-6, CAT. #12912S), interleukin-1β (IL-1β, CAT. #12242S), nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) p65 (CAT. #12629S), activator protein 1 (AP-1, CAT. #9165S), and mitogen-activated protein kinase (MAPK) family antibody (JNK, CAT. #9252S; p-JNK, CAT. #4668S; p38, CAT. #9212S; p-p38, CAT. #4511S) were provided by Cell Signaling Technology (Danver, MA, USA).

Techniques: