fig01

LPS-induced TLR4 neuroinflammatory signaling in CHME-5 microglial cells

Figure 1. LPS-induced NF-κB p65 activation. CHME-5 cells were exposed to LPS (0.1-1 μg/mL) or media alone at 37 °C for 30 min. A: nuclear lysates were subjected to SDS-PAGE electrophoresis and immunoblotted with NF-κB p-p65 (1:1,000), NF-κB p65 (1:1,000), and β-tubulin (1:1,000) antibodies; B: data is normalized to US and expressed as fold change, integrated density, (*P < 0.02) vs. 0.1 μg/mL, images are representative of 3 independent experiments (n = 3) for each treatment group; C: CHME-5 cells were exposed to LPS (0.001-10 μg/mL) or media alone at 37 °C for 30 min, cell viability absorbance was read at 492 nm, 3 independent experiments were performed in duplicate (n = 3) for each treatment group; D: CHME-5 cells were stimulated with LPS (1 μg/mL) at 37 °C for 10-270 min, nuclear extracts were analyzed for NF-κB p65 binding activity, (*P < 0.04, **P < 0.01) vs. US. Image is representative of 5 independent experiments (n = 5) for each treatment group. Bars for all groups are presented as mean ± SEM. LPS: lipopolysaccharide; NF-κB: nuclear factor-kappa B; SDS-PAGE: sodium dodecyl sulfate polyacrylamide gel electrophoresis; US: unstimulated

Neuroimmunology and Neuroinflammation
ISSN 2349-6142 (Online) 2347-8659 (Print)

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