Research Paper Volume 13, Issue 1 pp 1440—1457
NLRC4 gene silencing-dependent blockade of NOD-like receptor pathway inhibits inflammation, reduces proliferation and increases apoptosis of dendritic cells in mice with septic shock
Figure 5. Improved morphological changes in DCs after being cultured for 3 h, 3 d, 5 d, and 7 d and suppressed NLRC4 reduces DC proliferation. (A) Morphological changes of DCs observed under an inverted microscope (scale bar = 50 μm). (B) The expression of NLRC4 in DCs determined by RT-qPCR. (C) The induction of DC surface markers, CD80, CD86, and MHC II, detected by flow cytometry. (D) The DC apoptosis as indicative of OD values detected by flow cytometry. (E) The immunofluorescence labeling of NLRC4 and DC surface marker CD86 (scale bar = 25 μm). The bone marrow-derived DCs from the same group of mice were adopted in the in vivo experiments. * p < 0.05 vs. the sham group. † p < 0.05 vs. the CLP and NC-siRNA groups. Data comparison among multiple groups was analyzed by one-way ANOVA, followed by Tukey’s post-hoc test. Data at different time points were compared by repeated measures ANOVA, followed by Bonferroni test. The experiment was repeated 3 times independently.