en زیست شناسی ملکولی Molecular Biology مقالات اصلی Original Article <div style="text-align: justify;"><span style="font-size:10pt"><span style="text-justify:kashida"><span style="text-kashida:0%"><span style="line-height:normal"><span style="tab-stops:396.55pt"><span style="font-family:Calibri,sans-serif"><b><i><span lang="EN-GB" style="font-size:12.0pt"><span new="" roman="" style="font-family:" times=""><span style="color:black"><span style="letter-spacing:-.3pt">Background:</span></span></span></span></i></b> <span style="font-size:12.0pt"><span new="" roman="" style="font-family:" times=""><span style="color:black"><span style="letter-spacing:-.3pt">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.</span></span></span></span></span></span></span></span></span></span><br> <br> <span style="font-size:10pt"><span style="text-justify:kashida"><span style="text-kashida:0%"><span style="line-height:normal"><span style="tab-stops:396.55pt"><span style="font-family:Calibri,sans-serif"><b><i><span lang="EN-GB" style="font-size:12.0pt"><span new="" roman="" style="font-family:" times=""><span style="color:black"><span style="letter-spacing:-.3pt">Methods:</span></span></span></span></i></b><span style="font-size:12.0pt"><span new="" roman="" style="font-family:" times=""><span style="color:black"><span style="letter-spacing:-.3pt"> 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.</span></span></span></span></span></span></span></span></span></span><br> <br> <span style="font-size:10pt"><span style="text-justify:kashida"><span style="text-kashida:0%"><span style="line-height:normal"><span style="tab-stops:396.55pt"><span style="font-family:Calibri,sans-serif"><b><i><span lang="EN-GB" style="font-size:12.0pt"><span new="" roman="" style="font-family:" times=""><span style="color:black"><span style="letter-spacing:-.3pt">Results:</span></span></span></span></i></b><b> </b><span style="font-size:12.0pt"><span new="" roman="" style="font-family:" times=""><span style="color:black"><span style="letter-spacing:-.3pt">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.</span></span></span></span></span></span></span></span></span></span><br> <br> <span style="font-size:10pt"><span style="text-justify:kashida"><span style="text-kashida:0%"><span style="line-height:normal"><span style="tab-stops:396.55pt"><span style="font-family:Calibri,sans-serif"><b><i><span lang="EN-GB" style="font-size:12.0pt"><span new="" roman="" style="font-family:" times=""><span style="color:black"><span style="letter-spacing:-.3pt">Conclusion:</span></span></span></span></i></b><span style="font-size:12.0pt"><span new="" roman="" style="font-family:" times=""><span style="color:black"><span style="letter-spacing:-.3pt"> 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.</span></span></span></span></span></span></span></span></span></span></div>  CCL2, CCR2, CX3CL1, CX3CR1, Liver fibrosis. 350 358 http://rbmb.net/browse.php?a_code=A-10-1300-1&slc_lang=en&sid=1 Parisa Varjavand 100319475328460017990 100319475328460017990 No Department of Biology, Islamic Azad University Central Tehran Branch, Tehran, Iran. Ardeshir Hesampour hesampoor@azad.ac.ir 100319475328460017991 100319475328460017991 Yes Department of Biology, Islamic Azad University Central Tehran Branch, Tehran, Iran.