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Fig. 5 | Journal of Neuroinflammation

Fig. 5

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. 5

CXCR5 knockout reversed the alteration in hippocampal microglial M1/M2 polarization 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 densitometry of hippocampal Iba-1 on day 14 after CLP. b Representative micrographs of immunohistochemistry for Iba-1 in the hippocampal CA1 and the number of Iba-1-positive cells. Magnification, 200 × . Scale bar, 100 μm. Representative immunofluorescence micrographs and quantitation (n = 4 per group) after staining for c M1 marker iNOS and d M2 marker Arg-1 in the hippocampal CA1 region. Magnification, 200 × . Scale bar, 100 μm. *p < 0.05 vs. WT + sham; #p < 0.05 vs. WT + CLP. Arg-1 arginase-1, CLP cecal ligation and puncture, CXCR5 C-X-C chemokine receptor type 5, Iba-1 ionized calcium binding adaptor molecule-1, iNOS inducible nitric oxide synthase, WT wild-type

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