MFA, Extracted From Securidaca Inappendiculata Hassk, On Acute Liver Injury In Mice Model Of Carbon Tetrachloride And Mechanism Research

Objective: The purpose of this study was to establish CC14 to animal models of acute liver injury in mice, on the basis of observation of acute liver injury caused by CC14 and liver cell apoptosis, the MFA for liver injury in vivo animal models of liver function, and further explore MFA protection liver cell, alleviate the mechanism of liver injury.Methods : Will be 60 kunming mice were randomly divided into 6 groups, normal control group, model control group, positive control group, respectively(100 mg/kg) biphenyl double ester, MFA high dose group(200 mg/kg), MFA in dose(100 mg/kg), MFA, low dose group(50 mg/kg).In addition to the normal group and model group, the rest of the group dose lavage 7 days respectively, 1 times a day.1 hour after 7 day to fill the stomach, the model control group, positive control group and drug group with 0.5% CCl4- by intraperitoneal injection of peanut oil to l0ml/kg dose 1, acute CCl4 liver injury model.In the building after 24 hours, eyeball blood, remove the liver, spleen and detection of serum ALT, AST activity and liver homogenate MDA, SOD, gsh-px activity, liver tissue pathological changes were observed.At the protein level detection of normal control group, model control group, positive control group(100 mg/kg) biphenyl double ester, MFA group(100 mg/kg) in liver tissue of NOX4, the expression of phosphorylated P38 lightning and Caspase 3, using rt-pcr detection of liver tissue in the amount of the expression of NOX4 and Caspase 3 in.Results: Model group mice showed higher serum ALT, AST and liver tissue MDA, and liver tissue SOD, gsh-px decreased obviously.Methyl ferulic acid group(50 mg/kg dose, 100 mg/kg and 200 mg/kg) and positive control group compared with model group, the indicators of serum ALT, AST and liver tissue MDA decreased obviously, and the liver tissue SOD, gsh-px increased significantly, the difference was statistically significant(P < 0.05 or P < 0.01), liver pathological section shows that can improve the liver pathological damage, and a significant dose- effect relationship.The phosphorylated P38 lightning signals of protein levels in model group significantly enhanced, MFA group was much less signal.Protein imprinting experiments and rt-pcr showed that compared with model group and control group, after giving MFA can effectively reduce the expression of NOX4 inside liver, Caspase 3, statistically significant difference(P < 0.05 or P < 0.01).Conclusions: MFA has strong yards out the pharmacological effects of reactive oxygen species, can reduce liver cell peroxidation damage.The mechanisms may alleviate liver injury by cut NOX4 / ROS- p38 lightning MAPK signal axis, relieves the cells from oxidative stress injury.At the same time by inhibiting the expression of Caspase 3, liver cell inhibits apoptosis of liver cells provides the material basis for the normal liver cells regeneration, repair function.In conclusion, MFA has protective effect on acute liver injury in mice caused by CCl4.