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. 2021 Feb 5;8:627927. doi: 10.3389/fmed.2021.627927

Figure 4.

Figure 4

CCL2 was responsible for macrophages infiltration and differentiation into M2 phenotype during liver fibrosis. (A) Representative images of macrophage infiltration under different chemotaxis treatments including aHSC, aHSC+INCB, Rh CCL2 and medium. (B) Statistical analysis of the number of macrophages infiltration. The aHSC group vs. medium group, P < 0.01, aHSC+INCB group vs. aHSC group, P < 0.01. Rh CCL2 vs. medium group, P < 0.01. (C) The representative flow cytometry data of macrophage phenotypic change when exposed to CCL2 treatment with or without INCB. (D) CCL2 significantly up-regulated CD163 expression on macrophages; this effect could be blocked by INCB (100 ng/ml). (CCL2 group vs. M0 NC group, P = 0.008; CCL2 group vs. CCL2 + INCB group, P < 0.01). (E) CCL2 significantly up-regulated CD206 expression on macrophages, and this effect could be blocked by INCB (100 ng/ml). (CCL2 group vs. M0 NC group, P = 0.003; CCL2 group vs. CCL2 + INCB group, P < 0.01). These experiments were repeated at least three times.