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Objective: The high fat diet-induced fatty liver model, the preventive effect of non-alcoholic fatty liver of rats with experimental observation sesamin and explore its mechanism. Methods: 40 healthy male SD rats the adaptive feeding a normal diet for 3 days, were randomly divided into five groups according to body weight and initial cholesterol levels, normal control group, model group, sesamin low, medium and high dose group ( low, medium and high doses were 20, 40, and 80 mg / kg · d -1 ). Animals were sacrificed after 9 weeks, measured in serum and liver homogenates of total cholesterol (TC), triglyceride (TG), low density lipoprotein (LDL), high density lipoprotein (HDL), superoxide dismutase (SOD), malondialdehyde (MDA); vitality blood alanine aminotransferase (ALT) aspartate aminotransferase (AST) and liver homogenates lipoprotein lipase (LPL), hepatic lipase (HL) . RT-PCR analysis of liver tissue cholesterol 7α hydroxylase (CYP7A1) and hepatic cytochrome P450 (CYP) 2E1mRNA changes in expression levels; the liver histological observation liver pathology. Results: 1. Liver index of the model group was significantly higher than the control group (P <0.05) and low, Sesamin dose group the liver index higher fat model group (P <0.05), but no difference between the three dose groups . Hyperlipidemia model group, serum TC was significantly higher than the control group (P <0.05), sesamin in the high dose group TC lower than the model group (P <0.01); rats in each group TG was no significant difference ( P> 0.05); hyperlipidemia model group, HDL-C lower than the normal control group, the sesamin each dose group HDL-C was significantly higher than the model group (P <0.01); hyperlipidemia model group, LDL-C compared with normal control group (P <0.05), sesamin dose group LDL-C lower than the model group (P <0.01). Model group than the normal control group liver homogenates TC, TG, LDL-C were significantly increased (P lt; 0.05); higher lipid model group sesamin three dose groups TC, TG, LDL-C decreased (P lt; 0.05). TC, TG, LDL-C content with increasing dose of sesamin gradually decreased (P lt; 0.05) fat model group LPL, ALT activity was lower than the normal control group, the the sesamin high dose group a high fat control group LPL ALT activity increased (P lt; 0.05), no statistically significant difference among other groups; among the groups HL, AST was no significant difference. Hyperlipidemia model group, serum and liver FFA content higher than the normal control group (P lt; 0.05) the sesamin FFA contents of each dose group were lower than the model group (P lt; 0.05), but each dose group statistically significant. 6 hyperlipidemia model group and normal control group and sesamin dose serum SOD was no significant difference. Hyperlipidemia model group than in normal control group liver homogenate SOD activity decreased (P lt; 0.01), sesamin dose group SOD activity was high-fat model group were significantly increased (P lt; 0.01), and with the sesamin dose increased SOD activity increased. Hyperlipidemia model group, serum and liver MDA content compared with normal control group (P lt; 0.01); sesamin dose group MDA levels were lower than the high-fat model group (P lt; 0.01), sesamin dose groups The difference was not statistically significant. 7. Compared with the normal group, the the fat the model group CYP7A1mRNA expression level was significantly decreased (P lt; 0.05) sesamin group CYP7A1mRNA-expression levels were significantly higher than the model group (P lt; 0.05). Compared with the normal group, the the fat the model group CYP2E1mRNA expression level was significantly increased (P lt; 0.05) the sesamin group CYP2E1mRNA expression level was significantly lower than the model group (P lt; 0.05). Light microscopy observation observed: normal control group lobule structure is complete, clear, central venous large, thin-walled, liver cells were arranged hepatic cords arranged radially around the central vein; model liver tissue see severe fat change in liver cell volume increases, disorganized, cord-like structure is unclear, mixed vacuoles of cells filled with mainly large vacuoles, some watery changes associated with liver cell, the nucleus is pushed to the envelope, part of the nucleus dissolved and accompanied by inflammatory cell infiltration; Sesamin Group fatty degeneration of the number of liver cells and significantly compared with the model group, hepatocyte swelling is not obvious, higher fat group less intracellular lipid droplets and steatosis microvesicular nucleus centered no inflammatory cell infiltration. Fatty degeneration of the number of cells increased significantly, and no obvious inflammatory cell infiltration. Conclusion: sesamin can reduce fatty liver in rat liver lipid content, hinder initial role in the fight against the formation of fatty liver; significantly enhanced SOD activity and reduce oxidative metabolite MDA content significantly reduce CYP2E1mRNA expression, thus increase the antioxidant capacity, as well as suppression CYP2E1mRNA expression blocking the progress of the second attack on the liver cells in fatty lesions. Some role in prevention of non-alcoholic fatty liver.
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