Sesamin Prevention Of Nonalcoholic Fatty Liver Disease

Objective To study whether sesamin can prevent the development ofrats'nonalcoholic fatty liver disease.Methods 40 SD rats were randomly divided into 5 groups according tothe initial serum cholesterol and weight．The normal control group,model group,and three doses of seamine groups(20,40,80mg/kg·d^-1)．After 9 weeks,TC,TG,LDL,HDL in liver and sera were determined by biochemistry analysis,andthe malondialdehyde(MDA) and superoxidedismutase(SOD) activity of hepatictissue and sera were measured．FFA, AST, ALT in sera and LPL,HL in liver werealso measured．The expression levels of cholesterol 7αhydroxylase (CYP7A1) andCytochrome P4502E1 mRNA in liver tissue were measured by reversetranscriptase-polymerase chain reaction (RT-PCR)．The liver pathology wasobserved under the light microscope．Results1. Liver/body weight index of model group was increased significantly comparedwith normal group(P﹤0.05).Compared with model group ,the treatment groupswere decreased markedly(P﹤0.05).2. TC in sera of model group was increased significantly compared with normalgroup(P﹤0.05). Compared with model group, the middle and high dosestreatment groups were decreased markedly(P﹤0.05).TG had no significantdifferences. HDL in sera of model group was decreased significantly comparedwith normal group(P﹤0.05). Compared with model group, the treatmentgroups were increased markedly(P﹤0.05). LDL in sera of model group wasincreased significantly compared with normal group(P﹤0.05). Compared withmodel group, the treatment groups were decreased markedly(P﹤0.05)3. TC,TG,LDL in liver of model group were increased significantly compared withnormal group(P﹤0.05,). Compared with model group, the treatment groupswere decreased markedly(P﹤0.05)4. LPL and ALT in liver of model group were decreased significantly comparedwith normal group(P﹤0.05). Compared with model group, the high dosetreatment group were decreased markedly(P﹤0.05). HL and AST had nosignificant differences.5. FFAs in both sera and liver of model groups were increased significantly compared with normal group(P﹤0.05). Compared with model group, thetreatment groups were decreased markedly(P﹤0.05)6. SOD in sera had no significant differences. SOD in liver of model group wasdecreased significantly compared with normal group(P﹤0.01). Compared withmodel group, the treatment groups were increased markedly(P﹤0.01). MDA insera and liver of model group was increased significantly compared withnormal group(P﹤0.05). Compared with model group, the treatment groupswere decreased markedly(P﹤0.05).7. The expression of CYP7A1 mRNA in model group was decreased significantlycompared with that of normal group(P<0.05).Compared with model group, thetreatment groups were increased remarkably(P﹤0.05).The expression ofCYP2E1 mRNA in model group was increased significantly compared with thatof normal group(P<0.05). Compared with model group, the treatment groupswere decreased remarkably(P﹤0.05).8. Pathology observed by HE stain: Steatosis was not seen in controlled group,while severe lipid degeneration of liver were found in model group. Comparedwith model group, lipid degeneration in treatment groups were decreasedremarkably.Conclusions Sesamin can decrease fat in liver, increase the activity ofSOD, and decrease MDA and the expression of CYP2E1. So, sesamin can preventthe development of rats＇nonalcoholic fatty liver disease.