Bisdemethoxycurcumin Antagonistic Alzheimer's Disease Through Up-regulation Of Sirt1 And Anti-oxidative Stress

Objective This study was to investigate the concrete internal mechanism of bisdemethoxycurcumin antagonistic to alzheimer disease,to clear and definite that bisdemethoxycurcumin could increase the silent information adjustment factor 1(Sirt1)oxidation stress implementation antagonism of alzheimer's disease.Methods Our experiments are divided into two parts: the first part is to investigate whether bisdemethoxycurcumin has the effect of anti Alzheimer's disease in the vivo test.Firstly,normal mice and APP/PS1 mice was interfered with bisdemethoxycurcumin,learning and memory function was observed by the Morris water maze test and the Y maze test.Secondly Oxide dismutase(SOD)and glutathione(GSH)were observed to detect the level of oxidative stress.And then pathomorphology of the hippocampus in mice was detected by Nissl staining.Finally,the deposition of A? in the hippocampus of mice was detected by A? immunofluorescence staining and protein immunoblotting.The second part is to investigate whether the effect of bisdemethoxycurcumin on Alzheimer's disease is related to upregulated Sirt1 and then improve oxidative stress.Firstly,we injected Sirt1 inhibitor EX527 into the tail vein and detected the expression of Sirt1 in the hippocampus of mice by Western blotting.Then the APP/PS1 mice and APP/PS1 mice interfered by bisdemethoxycurcumin,they are injected by EX527 which is the inhibitors of Sirt1.Finally,we detected the learning and memory function ? oxidative stress level on the APP/PS1 mice and the APP/PS1 mice interfered by bisdemethoxycurcumin.Result1.The correct alternation rate of APP/PS1 mice treated with bisdemethoxycurcumin increased the correct alternation rate and the escape latancy shortened,indicating that the learning and memory function of APP/PS1 mice treated with bisdemethoxycurcumin was obviously improved.2.The APP/PS1 mice treated with bisdemethoxycurcumin decreased the activity of superoxide dismutase and increased the activity of glutathione enzyme in the control group,which showed that the oxidative stress level of APP/PS1 double transgenic mice with bisdemethoxycurcumin was obviously improved.3.The APP/PS1 mice treated with bisdemethoxycurcumin increased the number of Nissl corpuscles in the control group,the morphology of the neurons was more complete and the number of the cells in the hippocampus increased.It showed that APP/PS1 mice treated with bisdemethoxycurcumin improved the morphological structure of hippocampus.4.The A? deposition in the hippocampus of the APP/PS1 mice treated with bisdemethoxycurcumin was less than that in the control group,indicating that the A? toxicity of the APP/PS1 mice was reduced.5.The level of Sirt1 in the APP/PS1 mice treated with bisdemethoxycurcumin was higher than that in the control group.It indicated that bisdemethoxycurcumin could increase Sirt1 in the APP/PS1 mice.6.Inhibition of Sirt1 can improve the learning and memory ability and anti oxidative stress of the APP/PS1 mice induced by bisdemethoxycurcumin.Conclusion1.Bisdemethoxycurcumin can antagonize AD in vivo.2.bisdemethoxycurcumin antagonized AD by up-regulating the level of Sirt1 and then anti oxidative stress.