Study On The Anti-inflammation Mechanism Of Phytic Acid In Mptp-induced Parkinson’s Disease Model Of Mice

Objective: To investigate the effect of Phytic acid(PA) on the content of Tyrosine hydroxylase(TH) and ionized calcium bindingadaptor molecule-1(iba1), the activity of inducible nitric oxide synthase(i NOS), the expression of nuclear factor κB(NF-κB) and phosphorylated extracellular signal-regulated kinase(p-ERK) induced by1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine(MPTP) and then study the protective mechanism of PA on dopaminergic neurons.Methods: C57BL6 mice were divided into control group, MPTP destroy group and PA treatment groups treated with MPTP and PA. The movement coordination function was tested by the rotarod apparatus. The damage to the dopaminergic neurons in the SNpc and the the expression of inflammatory marker Iba-1 in microglial cells were detected by immunohistochemistry method. The activity of i NOS was measured by real-time quantitative RT-PCR, the protein content of nuclear factor κB(NF-κB) and phosphorylated extracellular signal-regulated kinase(p-ERK) were analyzed by Western blotting.Results: The value of assessment showed a substantial loss of nigral dopamine neurons and behavioral deficits in MPTP destroy group compared with the control group. The expression of iba1, NF-κB, p-ERK and the activity of i NOS were increased in MPTP destroy group compared with the control group. PA improved impairments of motor function, prevents the MPTP-induced neuron loss in PA treatment groups compared with the MPTP destroy group. The expression of iba1, NF-κB, p-ERK and the activity of i NOS were reduced by PA in PA treatment groups compared with the MPTP destroy group.Conclusion: PA can suppresses microglia activation induced by MPTP. It may inhibits apoptosis of dopaminergic neurons by attenuating inflammatory responses and the levels of NFκB and p-ERK in MPTP-induced Parkinson’s disease model of mice...