Skip to main content
Fig. 7 | Journal of Neuroinflammation

Fig. 7

From: CXCR5 down-regulation alleviates cognitive dysfunction in a mouse model of sepsis-associated encephalopathy: potential role of microglial autophagy and the p38MAPK/NF-κB/STAT3 signaling pathway

Fig. 7

CXCR5 knockdown restored p38MAPK-dependent autophagy in LPS-treated microglial cultures. Microglial cells were treated with CXCR5 siRNA. a Western blot and densitometry of CXCR5 in microglia at 24 h after CXCR5 siRNA administration. $p < 0.05 vs. cells treated without siRNAs. Microglial cells were treated with CXCR5 siRNA at 24 h before LPS treatment. Some cultures were also treated with p38MAPK inhibitor SB203580 or agonist P79350 at 1 h before siRNA administration. b Representative micrographs of immunohistochemistry for LC3 in microglia at 24 h after LPS treatment. Magnification, 200 × . Scale bar, 100 μm. c Calculation of LC3-positive area. d–h Western blot and densitometry of LC3, beclin-1, Atg-5 and p62, and the ratio LC3-II/LC3-I (n = 4 per group). *p < 0.05 vs. control; #p < 0.05 vs. LPS; &P < 0.05 vs. LPS + CXCR5 siRNA. Atg-5 autophagy-related gene-5, GAPDH glyceraldehyde-3-phosphate dehydrogenase, LC3 microtubule-associated protein 1 light chain 3

Back to article page

Journal of Neuroinflammation

ISSN: 1742-2094