Lutein Effect On Oxidative Damage And Related Genes Of D-gal Model In Mice

Objective:Lutein is one kind of natural carotenoid, its unique molecular structure have guaranted its antioxidant properties,it also has an important role in the prevention of macular degeneration, cataracts, and development of tumors,cardiovascular diseases,skin and eye protection.Oxidative stress is the imbalance state of oxidative and antioxidative system, will cause body injury,and related with some kind of diseases.In this study, We use D-gal mice model to investigate the mitigation of lutein on oxidative stress and its possible mechanism.Method:Kunming strain male mice were randomized into 4 groups:high lutein dose group (HL) and low lutein dose group(LL) 40,10 mg/kg. d, control group and model group. After 6 weeks,the content of reactive oxygen species (ROS),malondialdehyde (MDA),nitric oxide (NO) and activity of superoxide dismutase (SOD),total nitric oxide synthase (TNOS), inducable nitric oxide synthase(iNOS),constitutive nitric oxide synthase(cNOS)and mitochondrial Na+-K+-ATP ase,Ca2+-ATP ase in liver tissue and aspartate aminotransferase (AST),alanine aminotransferase (ALT) in serum were determined.The levels of toll-like receptor-4(TLR4) mRNA and hemeoxygenase-1(HO-1)mRNA, inducable nitric oxide synthase (iNOS)mRNA in hepatic tissue were determined using reverse transcription polymerase chain reaction(RT-PCR)technique.Results:(1)Model group ROS,MDA,serum ALT, AST content significantly higher than control group. Activities of SOD,Na+-K+-ATP ase,Ca2+-ATP ase significantly lower than control group. LL and HL group tissue ROS,MDA content,serum ALT,AST content level compared with model group were significantly decreased(p<0.05);HL group's activities of SOD,Na+-K+-ATP ase,Ca2+-ATP ase compared with model group were significantly increased(P<0.05).(2)Model group activities of TNOS and iNOS,cNOS and content of tissue NO were significantly increased (P<0.05);Activities of iNOS,cNOS and content of tissue NO in high lutein dose group compared with model group were significantly decreased respectively (P<0.05);Activities of TNOS in lutein groups compared with model group were significantly decreased (P<0.05).(3)Model group's HO-1 mRNA was significantly decreased, High lutein group's HO-1 mRNA level compared with model group was significantly increased(P<0.05).Model group's TLR4,iNOS mRNA level were significantly increased(P<0.05).TLR4,iNOS mRNA level of lutein dose groups was significantly decreased (P<0.05).Conclusion:Lutein can alleviate D-galactose induced oxidative stress in mice, reduce liver cell injury. The mechanism may be related to the effects of lutein in the following:(1)Scavenge oxygen free radicals,increase SOD enzyme,mitochondrial Na+-K+-ATPase,Ca2+-ATPase activity,protect mitochondria.(2) Lutein can inhibit the NO/NOS system, reduced the expression of iNOS and reduce NO levels.(3)Lutein can increase the expression of HO-1,reduce the expression of TLR4.Balance the body's oxidative stress state and inflammatory immune response.