the role of mesenchymal stem cells and imatinib in the process of liver fibrosis healing through ccl2-ccr2 and cx3cl1-cx3cr1 axes

Background: persistent liver damage contributes to the development of liver fibrosis, marked by an accumulation of extracellular matrix. macrophages play a pivotal role in this process, with the ccl2-ccr2 and cx3cr1-cx3cl1 axes serving as key regulators of macrophage recruitment, liver infiltration, and differentiation. in this study, utilizing a rat model of carbon tetrachloride (ccl4)-induced liver fibrosis, we aimed to investigate the impact of imatinib and bone marrow-derived mesenchymal stem cells (bm-mscs) on the expression of these axis.methods: sixteen sprague-dawley rats were divided into four groups: healthy, liver fibrosis, imatinib-recipient, and bm-msc-recipient. treatment effects were evaluated using histopathology and sirus-red staining. quantitative real-time pcr was employed to analyze changes in the expression of the genes ccl2, ccr2, cx3cl1, and cx3cr1.results: histopathological assessments revealed the efficacy of imatinib and bm-mscs in mitigating liver fibrosis. our findings demonstrated a significant reduction in ccl2 and ccr2 expression in both imatinib and bm-mscs treatment groups compared to the liver fibrosis group. conversely, the gene expression of cx3cl1 and cx3cr1 increased in both therapeutic groups compared to the liver fibrosis groups.conclusion: conclusion: the notable decrease in ccl2-ccr2 genes in both therapeutic groups suggests that bm-mscs and imatinib may contribute to a decline in inflammatory macrophages within the liver. the lower ccl2-ccr2 expression in imatinib-recipient rats indicates better efficacy in modulating the recruitment of inflammatory macrophages. the elevated expression of cx3cl1 in bm-msc-recipient rats suggests a greater impact on the polarization of ly6chigh (inflammatory) to ly6clow (anti-inflammatory) macrophages, warranting further investigation.