Abstract
The accumulated knowledge about the role of the CXCL12 chemokine in the initiation and development of liver fi brosis is insignifi cant and does not allow us to assess the potential of using the CXCL12 mRNA level as an independent marker of fi brogenesis and processes associated with fi brosis and cirrhosis. Thioacetamide modeling of liver fi brosis and cirrhosis in male Wistar rats showed a low level of CXCL12 mRNA expression (p = 0.0000) at all stages of fi brosis progression. At the beginning of the experiment (3 weeks), a decrease in the level of CXCL12 mRNA by 2.93 times (p = 0.0000) compared with the control group was revealed. After 3, 7 and 9 weeks, the level of gene expression decreased gradually (p = 0.0000). During the reorganization of the parenchyma of the organ and the formation of false hepatic nodules (11, 13 and 15 weeks), a certain stabilization of the level of gene expression was noted. Against the background of the total formation of pseudohepatic nodules and a pronounced diff use proliferation of connective tissue (17 weeks), the level of CXCL12 mRNA expression increased, but did not reach the level of control values. Based on our results, the level of CXCL12 mRNA is associated with the processes of fi brosis/cirrhosis and can act as an independent marker of fi brogenesis, but not cirrhosis of the liver against the background of toxic damage to it by thioacetamide. When conducting fundamental and preclinical studies to evaluate the eff ectiveness of drugs using this experimental model, the minimum allowable number of control points is considered to be three, namely: portal fi brosis (3 weeks), bridging fi brosis (5 weeks), the beginning of the process of transformation of liver fi brosis into cirrhosis (9 weeks).