[Effects of ellagic acid on inflammation and oxidative stress induced by AKT gene transfection in mice with fatty liver disease].

To study the effects of ellagic acid(EA)on inflammation and oxidative stress in mice with fatty liver disease induced by AKT gene transfection,the 20 female FVB mice were randomly divided into normal control group,model group and ellagic acid administration group(150,300 mg·kg~(-1)·d~(-1))(n=5).EA experimental groups and model group were using a high pressure into the tail vein transfection plasmid AKT.The next day,EA was started to administered continuously for 5 weeks after the AKT gene transfection,while the model group and the normal control group were given the same amount of saline.After the administration,the liver tissue and serum of mice were taken.HE and oil red O staining were using to observe the histopathological changes in liver;liver function to detect the serum and liver tissue as well as MDA and SOD levels;real-time quantitative PCR(RT-qPCR)was used to measure the mR-NA expression of NF-κB and TNF-α;Western blot and immunohistochemistry were used to measure the expression of NF-κB,TNF-αand COX-2 in liver tissue.RESULTS:: show that after AKT gene transfection,the model group had significant increase in the serum levels of AST,ALT,elevated the levels of MDA and decreased the levels of SOD in serum and liver tissue,aggravated histopathology degeneration and Liver inflammation,and significantly higher expression of NF-κB,TNF-α,IL-6,COX-2 and other inflammatory-related factors in liver tissue.EA administration group significant reductions in the serum levels of AST,ALT,and improved in hepatocyte fatty degeneration and liver inflammation,lower the levels of MDA and increased the levels of SOD in serum and liver tissue,and significant reductions in the expression of NF-κB,TNF-α,IL-6 and COX-2 in liver tissue.These results suggest that EA has obvious anti-inflammatory effect and inhibits oxidative stress and EA has a significant therapeutic effecton AKT gene inducing fatty liver,and the mechanism possibly by inhibiting inflammatory factors of NF-κB,TNF-α,IL-6,COX-2 and anti-oxidative stress-related.