Mechanism of the neuroprotective effect of injecting brain cells on ST36 in an animal model of Parkinson’s disease

Abstract

In Parkinson’s disease, the dopaminergic neurons of the brain are destroyed. Dopamine is an important neurotransmitter that acts on the basal ganglia of the brain, allowing precise body movement. In the early stages of Parkinson’s disease, levodopa appears to alleviate clinical symptoms; however, during long-term use, motor complications occur. There is no clear treatment or remedy for Parkinson’s disease; therefore, the development of novel therapies is urgently required. In the present study, mouse choroid plexus cells were transplanted into ST36 in a mouse model of Parkinson’s disease to determine whether the motor function could be restored. Pole tests showed changes in motor dysfunction in the mice. The athletic ability of the mice was significantly lowered after 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) injection and significantly increased after choroidal neuron cell treatment. Injection of di-alkyl indocarbocyanine (DiI) (as a trace substance) confirmed that the choroid plexus cells injected into acupuncture point ST36 were transferred to the brain. In the Parkinson’s disease model, choroid plexus cell injection into ST36 inhibited the decrease in tyrosine hydroxylase (TH) expression and decreased the activation of inflammatory factors mitochondrial cytochrome C oxidase (COX2) and inducible NO synthase (iNOS). Apoptosis factors Cytochrome C and BCL2 associated X, apoptosis regulator (BAX) levels were decreased and B-Cell CLL/Lymphoma 2 (BCL2) levels were increased. Taken together, these results suggest that the injection of choroid plexus cell at ST36 had neuroprotective effects in the Parkinson’s disease mouse model. The results suggest new possibilities for the treatment of Parkinson's disease.