ABSTRACT
Aim To explore changes of gut microbiota in experimental model rats with hyperuricemia-induced mild cognitive impairment. Methods The experimental rats were provided with a diet containing 2% W/W uric acid (UA) and 2% W/W oxonic acid for period ranging from 1 day to 12 weeks. Morris water maze, blood biochemical indexes and other auxiliary models were used to evaluate the experimental animal model. Changes of gut microbiota were studied by 16S rDNA high-throughput sequencing. Results Compared with control group, the amount of UA of rats was significantly elevated. In addition, the rats showed significantly reduced spatial learning and memory in an escape latency and probe trial. The diversity of gut microbiota in model rats changed, and the relative abundances of 14 species of gut microbiota changed markedly. The abundance of Butyrivibrio, Erysipelotrichia, Erysipelotrichales, Erysipelotrichaceae, Erysipelatoclostridium, Lachnoclostridium 5, Anaeroplasmatales, Anaeroplasmataceae and Anaeroplasma in model mice increased, while that of Dorea, RuminococcaceaeUCG_005, Butyricicoccus, Tyzzerella 3 and Parasutterella decreased. Conclusions The continuous increase of UA can regulate gut microbiota, and the imbalance of gut microbiota is closely related to the development of mild cognitive impairment, which may be one of the mechanisms of hyperuricemia-induced mild cognitive impairment.
ABSTRACT
Parkinson's disease is a common neurodegenerative disease in middle-aged and elderly people, in which the pathogenic factors are not yet clear. Genetics, dietary habits, environmental toxins, immunological abnormalities, inflammation and oxidative stress response, apoptosis, and mitochondrial dysfunctions which caused by a variety of physiological and biogenic changes are likely to exacerbate the occurrence of Parkinson's disease. In recent years, studies have shown that the activity of microglia is closely related to Parkinson's disease, and that the active microglia can promote the release of inflammatory factors, while the differentiation of dopamine neurons in the substantial nigra of midbrain area is also closely related to Parkinson's disease. As a histone H3K27me3 demethylase, JMJD3 is involved and affects the activity of microglia, which can regulate the polarization of microglia as well and affect the survival of dopaminergic neurons in the mesencephalon. This provides new methods and strategies for treating Parkinson' s disease. This paper summarizes the structure and function of JMJD3, as well as its role in neuro-inflammation mediated by microglia and its effect on neurons, and explores the functions and related research progress of JMJD3 in Parkinson's disease.
ABSTRACT
Aim To study the changes in endogenous differential metabolites of cerebral cortex and hippocampus extracts from cognitive dysfunction rats induced by hyperuricemia using * H nuclear magnetic resonance (