Objective To observe the effects of electro-acupuncture on the E-selectin and resistin protein expression in the hippocampus of rats of chronic stress depression;To explore the role and mechanism of electro-acupuncture in the micro-environment of brain with depression. Methods 40 Fourty rats were randomly divided into four groups:blank group, model group, model+EA group, and model+fluoxetine group by using chronic stress combined with solitary raising methods, 10 rats in each group. Electro-acupuncture intervention was used 1 hour before the modeling. Electro-acupuncture was given at points Baihui (Du 20) and Yintang (Extra) for twenty minutes (2 Hz, 0.6 mA) every day. Fluoxetine was given at the volume of 5 mL/kg, dosage of 10 mg/kg. E-selectin and resistin protein expression in hippocampus were determined by biotin label-based antibody array. Results Compared with the blank group, the protein expression of E-selectin and resistin in the model group increased (fold change=1.23, 1.22). Compared with the model group, E-selectin and resistin expression decreased (fold change=0.65, 0.62;fold change=0.76, 0.65). Conclusion Electro-acupuncture intervention could down-regulate E-selectin and resistin expression in the hippocampus of chronic stress depression model.

Whether direct manipulation of Parkinson's disease (PD) risk genes in the adult monkey brain can elicit a Parkinsonian phenotype remains an unsolved issue. Here, we used an adeno-associated virus serotype 9 (AAV9)-delivered CRISPR/Cas9 system to directly co-edit PINK1 and DJ-1 genes in the substantia nigras (SNs) of two monkey groups: an old group and a middle-aged group. After the operation, the old group exhibited all the classic PD symptoms, including bradykinesia, tremor, and postural instability, accompanied by key pathological hallmarks of PD, such as severe nigral dopaminergic neuron loss (>64%) and evident α-synuclein pathology in the gene-edited SN. In contrast, the phenotype of their middle-aged counterparts, which also showed clear PD symptoms and pathological hallmarks, were less severe. In addition to the higher final total PD scores and more severe pathological changes, the old group were also more susceptible to gene editing by showing a faster process of PD progression. These results suggested that both genetic and aging factors played important roles in the development of PD in the monkeys. Taken together, this system can effectively develop a large number of genetically-edited PD monkeys in a short time (6-10 months), and thus provides a practical transgenic monkey model for future PD studies.
Animals ; Brain ; CRISPR-Cas Systems/genetics* ; Dependovirus/genetics* ; Haplorhini ; Phenotype ; Protein Kinases/genetics*

Whether direct manipulation of Parkinson’s disease (PD) risk genes in the adult monkey brain can elicit a Parkinsonian phenotype remains an unsolved issue. Here, we used an adeno-associated virus serotype 9 (AAV9)-delivered CRISPR/Cas9 system to directly co-edit PINK1 and DJ-1 genes in the substantia nigras (SNs) of two monkey groups: an old group and a middle-aged group. After the operation, the old group exhibited all the classic PD symptoms, including bradykinesia, tremor, and postural instability, accompanied by key pathological hallmarks of PD, such as severe nigral dopaminergic neuron loss (>64%) and evident α-synuclein pathology in the gene-edited SN. In contrast, the phenotype of their middle-aged counterparts, which also showed clear PD symptoms and pathological hallmarks, were less severe. In addition to the higher final total PD scores and more severe pathological changes, the old group were also more susceptible to gene editing by showing a faster process of PD progression. These results suggested that both genetic and aging factors played important roles in the development of PD in the monkeys. Taken together, this system can effectively develop a large number of genetically-edited PD monkeys in a short time (6–10 months), and thus provides a practical transgenic monkey model for future PD studies.