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Fig. 3 | Journal of Neuroinflammation

Fig. 3

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. 3

CXCR5 knockout ameliorated sepsis-induced cognitive dysfunction in mice with sepsis-associated encephalopathy. WT mice or mice lacking the CXCR5 gene (CXCR5−/−) were subjected to sham surgery or CLP. a Western blot and b densitometry of hippocampal CXCR5 on day 14 after CLP. GAPDH was used as an internal control (n = 4 per group). Mice were assessed in the Morris water maze on day 14 after CLP, followed by the fear conditioning test. c Escape latency time, d time spent in the target quadrant, and e number of crossings over the target quadrant in the Morris water maze. f Freezing time in the fear conditioning test (n = 16 per group). *p < 0.05 vs. WT + sham; #p < 0.05 vs. WT + CLP. CLP cecal ligation and puncture, CXCR5 C-X-C chemokine receptor type 5, GAPDH glyceraldehyde-3-phosphate dehydrogenase, WT wild-type

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