FIGURE 5.

CCL7‐CCR1 interaction regulated macrophage phenotype through JAK2 /STAT1 pathway. (A) Protein abundance of JAK2, p‐JAK2, STAT1, p‐STAT1 and p‐JAK2/JAK2, p‐STAT1/STAT1 ratio in BMDMs incubated with rmCCL7 (100 ng/ml) and pre‐treated 1 hour with CCR1 antagonist‐BX471(1 μM and 10 μM). (B) M1 markers (iNOS, IL‐6, IL‐12A, IL‐12B, TNF‐α) mRNA level in BMDMs incubated with rmCCL7 alone or in combination with JAK2 inhibitor‐Fedratinib (1 μM) and STAT1 inhibitor‐Fludarabine (1 μM). (C) Pathological mechanism diagram of CCL7 in Ang II‐induced AAA. Values were represented as mean ± SEM; One Way ANOVA was used for data analysis in (A‐B) *P < .05; **P < .01; ***P < .001, respectively