Journal: BioMed Research International
Article Title: Pinocembrin Protects Human Brain Microvascular Endothelial Cells against Fibrillar Amyloid- β 1−40 Injury by Suppressing the MAPK/NF- κ B Inflammatory Pathways
doi: 10.1155/2014/470393
Figure Lengend Snippet: Effects of pinocembrin on MAPK pathways of hBMECs against fA β 1–40 -induced toxicity. (a) Images of phosphor-p38, phosphor-MK2, phosphor-SAPK/JNK, phosphor-c-Jun, and phosphor-ERK1/2 were acquired on the ArrayScan HCS Reader using the Cytoplasm to Nucleus Translocation BioApplication (×20). (b), (c), and (e) Values of Mean_CircRingAvgIntenDiff describe the capacity translocation of cytosolic phospho-p38, phospho-SAPK/JNK, and phospho-ERK1/2 to the nucleus and nuclear phospho-MK2 to the cytoplasm. (d) Nuclear average fluorescence intensity illustrates the expression of phosphor-c-Jun. Data are expressed as means ± SEM, n = 6, *** P < 0.001 versus control, # P < 0.05, ## P < 0.01, ### P < 0.001 versus fA β 1–40 .
Article Snippet: The primary antibody mixture containing antiphosphor-ERK1/2 (Thr202/Tyr204) mouse monoclonal (1 : 250, Cell Signaling, Beverly, MA, USA), antiphosphor-p38 (Thr180/Tyr182) rabbit polyclonal (1 : 400, Cell Signaling), anti-phosphor-MAPKAP kinase-2 (MK2) (Thr334) rabbit polyclonal (1 : 200, Cell Signaling), anti-phosphor-SAPK/JNK (Thr183/Tyr185) mouse monoclonal (1 : 400, Cell Signaling), anti-phosphor-c-Jun (Ser73) mouse monoclonal (1 : 200, Cell Signaling), or anti-NF- κ B p65 rabbit polyclonal (1 : 250, Invitrogen, Carlsbad, CA, USA) antibodies in PBS was incubated at 4°C overnight.
Techniques: Translocation Assay, Fluorescence, Expressing, Control