Expression of Mindin, a pattern recognition molecule, in a mouse model of acute liver injury induced by carbon tetrachloride / 临床肝胆病杂志

ABSTRACT

ObjectiveTo investigate the dynamic expression of Mindin protein in mice with acute liver injury induced by carbon tetrachloride (CCl4) and its mechanism of action. MethodsA total of 48 male C57B1/6 mice were selected and divided into experimental group (n=40) and control group (n=8). The mice in the experimental group were given intraperitoneal injection of CCl4 olive oil to induce acute liver injury, and the liver tissue was collected for pathological observation at 6, 12, 24, 48, and 72 hours after modeling. The mice in the control group were given intraperitoneal injection of olive oil. Western blot was used to measure the protein expression of Mindin and its change trend, and quantitative real-time PCR was used to measure the mRNA expression of Mindin. The t-test was used for comparison of continuous data between two groups. ResultsAbnormal liver structure was observed after liver injury was induced by CCl4, with the most significant pathological change at 48 hours. There was a low protein expression level of Mindin within 12-72 hours after the injection of CCl4. The mRNA expression of Mindin reached the lowest level at 12 hours after CCl4 injection and there was a significant difference between the experimental group and the control group at this time point (0.183±0.105 vs 1.023±0.247, t=8.841, P＜0.01); then there was a gradual increase in the mRNA expression of Mindin, and at 48 and 72 hours, the mRNA expression of Mindin in the experimental group was more than 2 times that in the control group (48 hours 2.548±0.775 vs 1.023±0.247, t=5.428, P＜0.01; 72 hours 2.699±0995 vs 1.023±0.247, t=4.621, P＜0.01). ConclusionThere is a significant change in Mindin protein during the process of acute liver injury induced by CCl4 in mice, which is characterized by the downregulation of protein expression and the regulation of post-transcriptional mRNA level, suggesting that Mindin may play an important role in the process of acute liver injury induced by CCl4.