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Fig. 4 | Journal of Neuroinflammation

Fig. 4

From: Systemic pro-inflammatory response facilitates the development of cerebral edema during short hypoxia

Fig. 4

Inflammation induced increased AQP4 expression via the NF-κB and MAPKs pathway. a Astrocytes pre-treated with or without PDTC were treated with LPS, TNF-α, or IL-1β for 2 h, followed by staining with specific p65 antibody (n = 3). b p65 translocation into cell nuclei (%) after treatment with LPS, TNF-α, or IL-1β for 2 h. c AQP4 protein levels in astrocytes treated with LPS for 12 h after pre-treatment with or without PDTC (n = 3). d Water permeability of cells after LPS or LPS + PDTC treatment (n = 100). **P < 0.01; ***P < 0.001 compared with control; ## P < 0.01;### P < 0.001 compared with LPS 12 h. e Phosphorylated levels of ERKs and p38 in astrocytes treated with LPS, TNF-α, or IL-1β for 0.5 h were increased (n = 3). ***P < 0.001, compared with control. f AQP4 mRNA changes measured by RT-PCR in astrocytes treated with LPS for 8 h after pre-treatment with p38 inhibitor, ERK1/2 inhibitor, JNK inhibitor (n = 3). ***P < 0.001 compared with control; ## P < 0.01 compared with LPS treatment. g Water permeability changes of astrocytes pre-treated with p38 inhibitor, ERK inhibitor, JNK inhibitor, p300 inhibitor, or transfected with p300 siRNA then exposure to LPS for 12 h (n = 100). ***P < 0.001 compared with control; ### P < 0.001 compared with LPS 12 h. All the data are presented as mean ± SD

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