Study On The Mechanism Of The Effect Of Atorvastatin Though Nrf2/ARE Signal Pathway On EAE Mice And Apoptosis

Research backgroundMultiple sclerosis is a complex central nervous system autoimmune disease, its causes are complex and diversity, oxidative stress is one of the important inducing factors. It can induce oxidative damage to the central nervous system and affect the normal function of the central nervous, even lead to the apoptosis of nerve cells. Atorvastatin is a common lipid lowering drug, it has good anti-oxidation action, this study was to explore the mechanism of atorvastatin on multiple sclerosis, Nrf2/ARE is an important endogenous antioxidant antioxidant response system, which plays an important role of antioxidant stress in the in vivo, the experimental autoimmune, encephalomyelitis multiple sclerosis is a classic animal model.ObjeetivTo study the impact of atorvastatin on EAE model Nrf2/ARE pathway.Methods1.The H2O2 content of the brain cells was detected in each group mice by ELISA; 2.The MDA/HO-1/GSH content of the brain cells was detected in each group mice by ELISA; 3. The Nrf2 relative content of the brain cells was detected in each group mice by RT-PCR; 4. The nulcus Nrf2 relative content of the brain cells was detected in each group mice by immunohistochemistry; 5. The Caspase-3 content of the brain cells was detected in each group mice by WB.ResultsThe content of H2O2 in the brain tissue of mice in EAE model group was more than that in the control group, the difference was statistically significant(P< 0.05), the content of H2O2 in brain tissue of mice in AT group was more than that in EAE model group, the difference was statistically significant (P< 0.05); the content of MDA in brain tissue of mice in EAE model group was more than that in the control group, the difference was statistically significant (P< 0.05), the content of MDA in brain tissue of mice in AT group was more than that in EAE model group, the difference was statistically significant (P< 0.05), the control group was lower than that of HO-1 and GSH content in brain tissue of mice in EAE model group, the difference was statistically significant (P< 0.05), HO-1 and GSH in the brain tissue of AT mice was more than that EAE model group, the difference was statistically significant (P< 0.05); the relative expression of Nrf2 in EAE model mice brain tissue and the content of mRNA is lower than that of the control group, the difference was statistically significant (P< 0.05), the relative expression of the mRNA Nrf2 in brain tissue of mice in AT group was higher than that in EAE model group, the difference was statistically significant (P< 0.05);Nuclear Nrf2 content in brain tissue of mice in EAE model group was more than that in the control group, the difference was statistically significant (P<0.05), The content of AT in brain tissue of mice nucleus of Nrf2 is higher than that of the EAE model group, the difference was statistically significant (P< 0.05);5.EAE in brain tissue of mice in the model group was higher than that in control group, the difference was statistically significant (P< 0.05), Relative expression of Caspase-3 in the brain tissue of mice in AT group was less than that in EAE model group, the difference was statistically significant (P< 0.05)ConclusionsAtorvastatin can inhibit oxidative stress via the Nrf2/ARE, and thus inhibit the apoptosis of nerve cells, it may to the inhibitory effect on autoimmune encephalomyelitis up.