Effects of Ginseng Protein on Gut Microbiota and BDNF/TrkB Signaling Pathway in Alzheimer s Disease Mice

[Objectives] To investigate the effects of ginseng protein on gut microbiota and BDNF/TrkB signaling pathway in Alzheimer s disease (AD) mice. [Methods] D-galactose/AlCl 3 co-induction was used to establish AD model, and mice were randomly divided into normal group 1, normal group 2, model group 1, model group 2, ginseng protein group, and microbiota transplantation group. Morris water maze experiment was used to evaluate learning and memory ability, and Western blot method was used to detect the expression of APP, p-Tau, BDNF, TrkB, p-TrkB proteins in brain tissue, and 16S rDNA was used to detect diversity of fecal microbiota. [Results] Ginseng protein and microbiota transplantation can shorten the escape latency of mice ( P <0.05), increase the number of crossing platforms ( P <0.05), reduce the expression of APP and p-Tau proteins in brain tissue ( P <0.05, P <0.01), increase the expression of BDNF, p-TrkB, p-TrkB/TrkB proteins ( P <0.05, P <0.01), and reduce the abundance of Alloprevotella, Ruminococcaceae _UCG-014, Prevotellaceae _UCG-001, and Ruminococcus _1 ( P <0.05, P <0.01). [Conclusions] The action mechanism of ginseng protein anti AD may be through regulating gut microbiota diversity and activating the BDNF/TrkB signaling pathway.

ω-3PUFAs Prevent MK-801-induced Cognitive Impairment in Schizophrenic Rats via the CREB/BDNF/TrkB Pathway

This study was to determine the protective effect of ω-3 polyunsaturated fatty acids（ω-3PUFAs） on MK-801-induced cognitive impairment in schizophrenia（SZ） rats and the underlying mechanism. A rat model of schizophrenia was induced by MK-801. The cognitive function of rats was assessed using a Morris water maze. The number of hippocampal neurons was measured by Nissl staining. The expression of CREB, p-CREB, BDNF, TrkB, p-TrkB, AKT, p-AKT, ERK, and p-ERK in the hippocampus of rats was detected by Western blotting. The results showed that ω-3PUFAs attenuated MK-801-induced cognitive impairment and hippocampal neurons loss, reversed the injury of the CREB/BDNF/TrkB pathway induced by MK-801, and antagonized MK-801-induced down-regulation of p-AKT and p-ERK in the hippocampus of rats. In conclusion, ω-3PUFAs enhances the CREB/BDNF/TrkB pathway by activating ERK and AKT, thereby increasing the synaptic plasticity and decreasing neuron loss, and antagonizing MK-801-induced cognitive impairment in schizophrenic rats.

Porcine placental peptides improve neuroblast proliferation and differentiation via enhancement of TrkB and BDNF levels in D-glatacose-induced mouse aging model

Aging affects the nervous system as well as other organs.In our study,we aimed to study the pharmacological effects and mechanism of porcine placental peptides(PPP)in aging process,and to observe the changes of neuroblast proliferation and differentiation as well as partial gene expression in hippocampus of D-galactose-induced aged mouse.Based on the analysis of experimental results,it was confirmed that PPP significantly improved neurobalst proliferation and differentiation in the mouse hippocampal DG by ki-67 and DCX immunohistochemistry.This result showed that PPP had anti-aging effects on D-galactoseinduced aging mouse model.Moreover,we observed up-regulated expressions of BDNF and TrkB proteins and down-regulated expressions of Caspase 3,8,and 9 proteins in the PPP-treated mouse hippocampus.Therefore,our results showed that PPP obviously improved neuroblast proliferation and differentiation,and its anti-aging effect might berelated to down-regulation of apoptosis-related proteins,including Caspase 3,8,and 9,via BDNF/TrkB pathway.Our findings provided valuable evidence for its applications in the health and medicine sectors.