ABSTRACT
OBJECTIVE: Parkinson's disease (PD) is a chronic neurodegenerative disease involving non-motor symptoms, of which gastrointestinal disorders are the most common. In light of recent results, intestinal dysfunction may be involved in the pathogenesis of PD. Electroacupuncture (EA) has shown potential effects, although the underlying mechanism remains mostly unknown. We speculated that EA could relieve the behavioral defects of PD, and that this effect would be associated with modulation of the gut microbiota. METHODS: Mice were randomly divided into three groups: control, PD + MA (manual acupuncture), and PD + EA. MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) was used to establish the mouse model of PD. Rotarod performance tests, open field tests, and pole tests were carried out to assess motor deficiencies. Immunohistochemistry was conducted to examine the survival of dopaminergic neurons. 16S ribosomal RNA (rRNA) gene sequencing was applied to investigate the alterations of the gut microbiome. Quantitative real-time polymerase chain reaction (PCR) was performed to characterize the messenger RNA (mRNA) levels of pro-inflammatory and anti-inflammatory cytokines. RESULTS: We found that EA was able to alleviate the behavioral defects in the rotarod performance test and pole test, and partially rescue the significant loss of dopaminergic neurons in the substantia nigra (SN) chemically induced by MPTP in mice. Moreover, the PD + MA mice showed a tendency toward decreased intestinal microbial alpha diversity, while EA significantly reversed it. The abundance of Erysipelotrichaceae was significantly increased in PD + MA mice, and the alteration was also reversed by EA. In addition, the pro-inflammatory cytokines interleukin (IL)-6 and tumor necrosis factor (TNF)-α were substantially increased in the SN of PD + MA mice, an effect that was reversed by EA. CONCLUSION: These results suggest that EA may alleviate behavioral defects via modulation of gut microbiota and suppression of inflammation in the SN of mice with PD, which provides new insights into the pathogenesis of PD and its treatment.
Subject(s)
Electroacupuncture , Gastrointestinal Microbiome , Parkinson Disease/microbiology , Parkinson Disease/therapy , Animals , Bacteria/classification , Bacteria/genetics , Bacteria/isolation & purification , Behavior, Animal , Cytokines/genetics , Cytokines/metabolism , Disease Models, Animal , Dopaminergic Neurons/metabolism , Humans , Interleukin-6/genetics , Interleukin-6/metabolism , Male , Mice , Mice, Inbred C57BL , Parkinson Disease/metabolism , Parkinson Disease/psychology , Tumor Necrosis Factor-alpha/genetics , Tumor Necrosis Factor-alpha/metabolismABSTRACT
OBJECTIVE: To evaluate the molluscicidal effect of the plastic film mulch covering method. METHODS: In the barren land with a lot of Oncomelania hupensis snails, 3 experimental groups were set up, in which respectively using 3 different methods: a simple plastic film mulch covering method, film assisted with ammonium bicarbonate, and film assisted with amine molluscicide. In the canals, two experimental groups were set up, in which respectively using 2 different methods: simple plastic film mulch covering method and film assisted with ammonium bicarbonate. In above-mentioned areas, obstacles were cleared artificially. In each experiment group, 4 observation spots were set up, and 100 living snails were pot in each spot, and then, the plastic film mulch was evenly covered. The status of the snails was observed 3, 7, 15 and 30 days after the intervention. RESULTS: In the barren land, the snail death rates of the simple plastic film group were 20.77% and 96.92% 15 days and 30 days after the intervention, respectively. The snail death rate of the film assisted with amine molluscicide group was 80.46% 3 days after the intervention. In all the experiment groups, the snail death rates were from 96.92 to 100% 30 days after the intervention. CONCLUSION: The plastic film mulch covering method has a great molluscicide effect in the hill subtype and water network type of schistosomiasis epidemic areas.