ObjectiveObjective To summarize the latest research progress on the copper death mechanism in metabolic associated fatty liver disease (MAFLD) and to provide new avenues for the treatment of MAFLD. MethodsWe reviewed recent domestic and international research on copper and copper death in MAFLD, and summarized the role of copper death mechanisms in the pathogenesis of MAFLD and related treatments. ResultsCopper death is primarily caused by abnormal intracellular copper accumulation binding to acylated proteins in the tricarboxylic acid cycle, leading to protein oligomerization, downregulation of iron-sulfur cluster protein expression, triggering a toxic stress response, and ultimately cell death. The occurrence and progression of MAFLD are closely associated with genes associated with the copper death pathway. Imbalanced copper metabolism can lead to insulin resistance, causing abnormalities in blood glucose and lipid metabolism, promoting fat accumulation in the liver, and ultimately contributing to the development of MAFLD. Targeting genes involved in the copper death pathway can delay the progression of MAFLD. ConclusionThe occurrence and progression of MAFLD are closely linked to the copper death signaling pathway, with copper metabolism imbalance as a core component. This pathway not only directly leads to hepatocyte death but also triggers insulin resistance and abnormal lipid metabolism, jointly driving the progression of MAFLD. Therefore, targeted regulation of the copper death pathway is a novel therapeutic strategy to slow the progression of MAFLD.
Objective To investigate the effect on expression regulation of calmodulin-dependent kinases casades (CaMK) Ⅱ on liver function after liver transplantation in rats. Methods Allogeneic orthotopic liver transplantation model was established by using the classic two-cuff method. The lentiviral expression systems of CaMKⅡγ protein and CaMKⅡγ shRNA were constructed. The lentiviral vector expressing CaMKⅡγ shRNA and the lentiviral vector expressing CaMKⅡγ protein were perfused into the rat after liver transplantation respectively, and the corresponding blank vector and normal saline were perfused into the control group at the same time. The serum levels of ALT and AST were measured at different time points of inferior vena cava blood in rats. Results The serum ALT and AST levels were debased in the after transplantation rats whose lentiviral vector expressing CaMKⅡγ shRNA (P<0.05). The serum ALT and AST levels were raised in the after transplantation rats whose lentiviral vector expressing CaMKⅡγ protein (P<0.05). There were no significant difference of serum ALT and AST levels between the blank control group and the saline group (P>0.05). Conclusion Specific blocking of CaMK Ⅱ signaling pathway can effectively reduce the serum ALT and AST levels after liver transplantation in rats, and enhanced CaMK Ⅱ signaling pathway increases the serum ALT and AST levels after liver transplantation in rats.
ObjectiveTo improve the calculation method of the sum of residual hepatic lobe volume and total liver volume after partial hepatectomy in rats.MethodsOne hundred and thirty-five SD rats of different body sizes were divided into five groups by completely random design. The body length, tail length, chest circumference, body weight and length of hepatic triangle lobe of the rats were measured before surgery. Then, according to the classic Higgins and Anderson methods, different lobectomies of liver were performed for each group: middle lobe + left inner lobe, left outer lobe, bilateral papillary lobe, triangular lobe, and right lateral lobe were removed; the proportion of theoretical liver resection in each group was 38.1%, 30.1%, 7.9%, 7.8% and 15.3%, respectively. The actual liver resection volume and residual liver volume were measured after surgery. we finally analyzed statistical differences of liver volume calculated by different indirect methods. In addition, the correlation analysis and regression analysis were conducted between the preoperative measured rat body surface parameters and the measured whole liver volume, so as to explore a more simple and accurate volume measurement method.ResultsThe actual proportion of liver resection in each group was 35.0%, 29.2%, 7.1%, 4.9% and 12.0%, respectively. Compared with the residual liver lobe volume actually measured, that calculated by using the indirect method of substitution of the theoretical liver resection proportion was statistically different in all the other four groups except the left outer lobe group. However, there was no statistical difference between the residual liver lobe volume actually measured and that calculated by the actual liver resection proportion in the 5 groups. In addition, in the preoperative measurement of 5 kinds of basic parameters of rats, the body length has the best correlation with whole liver volume, and the regression equation is \begin{document}$\hat Y = - 27.667 + 0.899X$\end{document}.ConclusionsThe liver volume calculated by indirect method using the actual liver resection proportion, compared with the theoretical liver resection proportion, is more accurate. Compared with the body weight, the body length has the better correlation with whole liver volume.