Fig. 4

CXCR5 knockout restored hippocampal autophagy in mice with sepsis-associated encephalopathy. WT mice or mice lacking the CXCR5 gene (CXCR5^−/−) were subjected to sham surgery or CLP. a Representative transmission electron micrographs of the hippocampus show zoomed-in views (magnification, 5000 × ; Scale bar, 500 nm) of full image of a cell (magnification, 2000 × ; Scale bar, 2000 nm). Arrows indicate autophagosome. b Representative immunofluorescence micrographs showing LC3 in the hippocampal CA1 region. Magnification, 200 × . Scale bar, 100 μm. c Quantification of immunofluorescent cells staining positive for LC3. d–h Western blot and densitometry of hippocampal LC3, beclin-1, Atg-5 and p62, and the ratio of LC3-II/LC3-I. GAPDH was used as an internal control (n = 4 per group). *p < 0.05 vs. WT + sham; ^#p < 0.05 vs. WT + CLP. Atg-5 autophagy-related gene-5, CLP cecal ligation and puncture, CXCR5 C-X-C chemokine receptor type 5, GAPDH glyceraldehyde-3-phosphate dehydrogenase, LC3 microtubule-associated protein 1 light chain 3, WT wild-type