Objective To investigate the effect of S-adenosylmethionine (SAM) on mitochondrial injury that was induced by ischemia-reperfusion in rat liver. Methods Fifty-four rats were randomly divided equally into 3 groups: control group, ischemia-reperfusion group (I/R group), and SAM-treated group (SAM group). Hepatic ischemia had been only lasted for 30 min by obstructing the blood stream of hepatic portal vena (the portal vena was only separated but not obstructed in control group). The rats of SAM group received SAM intraperitoneally 2 h prior to ischemia. Blood samples of each group were collected from the inferior cava vena at 0, 1 and 6 h after reperfusion and the serum levels of AST and ALT were detected. Mitochondrial super oxidedismutase (SOD), malondialdehyde (MDA), adenosine triphosphate (ATP) and energy charge (EC) in samples of liver tissue were detected, and the mitochondrial ultrastructure was observed with electronmicroscope. Results The serum levels of AST, ALT and mitochondrial MDA at 0, 1 and 6 h after reperfusion in the I/R group were significantly higher than those in the control group, whereas the levels of mitochondrial SOD, ATP and EC were significantly lower than those in the control group (P＜0.01). Except the value of 0 h, when it comes to SAM group, the levels of AST, ALT and mitochondrial MDA were significantly lower (P＜0.05) and the levels of mitochondrial SOD, ATP and EC were significantly higher (P＜0.05, P＜0.01) than those in the I/R group, respectively. The mitochondrial ultrastructure was injured obviously in I/R group when compared with that in control group. The number of mitochondria decreased and the mitochondria swelled, making the crista became obscure and the density of matrix became lower. The above changes in SAM group were less obvious when compared with those in I/R group. Conclusion SAM may protect mitochondrion against hepatic ischemia injury, since it may prevent mitochondrial lipid peroxidation, increase ATP, and eventually improve energy metabolism after ischemia-reperfusion.
Objective To investigate the promoting effect of S-adenosyl-homocysteine hydrolase (AHCY) on the proliferation of lung cancer cells and its regulatory mechanism on the expression of methionine adenosyltransferase 1A (MAT1A). Methods Wayne plot analysis was performed on four lung cancer data chips, including GSE103512, GSE18842, GSE20189, and GSE102286, to screen for differentially expressed key genes. Protein immunoprecipitation assay was used to detect the interaction between AHCY and MAT1A. pAdTrack-CMV-NC+pCV702-NC (NC), pAdTrack-CMV, and pAdTrack-CMV+pCV702 were transfected into A549 and PC9 cells, respectively. The cell proliferation, apoptosis, the mitochondrial membrane potential, the ROS levels in cells, the total RNA methylation levels in cells, and the expression of AHCY and MAT1A in cells were detected, sequentially. Results The statistical analysis identified AHCY and MAT1A were the key differentially expressed genes across the four datasets. Co-immunoprecipitation experiments confirmed a direct interaction between AHCY and MAT1A in lung cancer (P<0.05). Upregulation of the expression of AHCY could significantly increase the proliferation of A549 and PC9 cells, decrease the cell apoptosis, increase the mitochondrial membrane potential, alleviate the intracellular reactive oxygen species levels, and decrease the total RNA methylation levels, while MAT1A overexpression partially reversed the promoting effects of AHCY on lung cancer cells. All differences were statistically significant (all P<0.05). Conclusions The expression of AHCY is significantly increased in lung cancer, while the expression of MAT1A is significantly decreased in lung cancer. High expression of AHCY can promote the cancer cell proliferation and affect total RNA methylation, while downregulate the expression of MAT1A in lung cancer cells.
