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Glycyrrhizic acid improves cognitive levels of aging mice by regulating T/B cell proliferation

ABSTRACT: We implemented transcriptomic analyses of blood of 12M mice; These mice with the treatment of Glycyrrhizic acid for 6 weeks.

ORGANISM(S): Mus musculus

PROVIDER: GSE146239 | GEO | 2020/06/18

REPOSITORIES: GEO

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Glycyrrhizic acid improves cognitive levels of aging mice by regulating T/B cell proliferation

Project description:Glycyrrhizic acid improves cognitive levels of aging mice by regulating T/B cell proliferation

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Glycyrrhizic Acid Improves Cognitive Levels of Aging Mice by Regulating T/B Cell Proliferation.

Project description:Glycyrrhizic acid (GA) is the substance with the highest content of triterpenoid saponins that can be extracted from licorice, and has anti-inflammatory, neuroprotective, and anticancer functions, among others. The aim of this study was to investigate the protective effect of GA on cognitive decline in middle-aged mice and explore its mechanisms. We injected GA by the tail vein of C57BL/6 mice and measured their cognitive levels using the Morris water maze. The Morris water maze results demonstrated that GA improved learning and memory abilities in middle-aged mice. Furthermore, the RNA-sequencing and flow cytometric analyses revealed that GA could increase T and B cells. We then confirmed the relationship between cognition and the immune system in the immune-deficient B-NDG mouse model. Our results suggest that GA improves cognition in aging mice by regulating T/B cell proliferation.

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Licochalcone A activate glycolysis by via PI3K / AKT pathway to play an anti-aging effect on adipose stem cells and aging mice [hippocampus]

Project description:We implemented transcriptomic analyses of hippocampus of 12M mice; These mice with the treatment of Licochalcone A for 30 days.

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Glycyrrhizic Acid Inhibits Myeloid Differentiation of Hematopoietic Stem Cells and Improves Cognition in Aged Mice by Binding to the S100 Calcium-Binding Protein A8 [HSC+GA RNA-seq]

Project description:Glycyrrhizic acid (GA) has numerous biological activities, but the mechanism by which it regulates the immune system and improves cognition in aged mice remains unclear. In this study, we analyzed single-cell sequencing data of peripheral blood mononuclear cells from young mice, aged mice, and GA-treated aged mice, and found that GA reduced senescence-induced increases in macrophages and neutrophils, and increased numbers of lymphoid lineage subpopulations specifically reduced by senescence. In vitro, GA significantly promoted differentiation of Lin-CD117+ hematopoietic stem cells toward lymphoid lineages, especially CD8+ T cells. Moreover, GA inhibited differentiation of CD4+ T cells and myeloid (CD11b+) cells by binding to the S100 calcium-binding protein 8 (S100A8). Overexpression of S100A8 in Lin- CD117+ hematopoietic stem cells enhanced cognition in aged mice and in immune reconstited severely immunodeficient B-NDG mice. Collectively, our results suggest that GA exerts anti-aging effects by binding to S100A8 to remodel the immune system of aged mice. We implemented transcriptomic analyses of rHSC treated with GA 24 hours

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Glycyrrhizic Acid Inhibits Myeloid Differentiation of Hematopoietic Stem Cells and Improves Cognition in Aged Mice by Binding to the S100 Calcium-Binding Protein A8 [OEA8-67-69 RNA-seq]

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Akkermansia muciniphila Membrane Protein Improves Cognitive Function in Aged Mice by Reducing IL-6 Expression

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Licochalcone A improves the cognitive ability of mice by regulating T- and B-cell proliferation.

Project description:Licochalcone A (LA), a flavonoid found in licorice, has anticancer, antioxidant, anti-inflammatory, and neuroprotective properties. Here, we explored the effect of injecting LA into the tail vein of middle-aged C57BL/6 mice on their cognitive ability as measured by the Morris water maze (MWM) test and cerebral blood flow (CBF). The related mechanisms were assessed via RNA-seq, and T (CD3e+) and B (CD45R/B220+) cells in the spleen and whole blood were quantified via flow cytometry. LA improved the cognitive ability, according to the MWM test results, and upregulated the CBF level of treated mice. The RNA-seq results indicate that LA affected the interleukin (IL)-17 signaling pathway, which is related to T- and B-cell proliferation, and the flow cytometry data suggest that LA promoted T- and B-cell proliferation in the spleen and whole blood. We also performed immune reconstruction via a tail vein injection of lymphocytes into B-NDG (NOD-PrkdcscidIl2rgtm1/Bcge) mice before treating them with LA. We tested cognitive ability by subjecting these animals to new object recognition tests and quantified the splenic and whole blood T and B cells. Cognitive ability improved after immune reconstruction and LA treatment, and LA promoted T- and B-cell proliferation in the spleen and whole blood. This study demonstrates that LA, by activating the IL-17 signaling pathway, promotes T- and B-cell proliferation in the spleen and whole blood of mice and improves cognitive ability. Thus, LA may have immune-modulating therapeutic potential for improving cognition.

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Glycyrrhizic Acid Inhibits Myeloid Differentiation of Hematopoietic Stem Cells and Improves Cognition in Aged Mice by Binding to the S100 Calcium-Binding Protein A8 [scRNA-seq]

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Glycyrrhizic Acid Inhibits Myeloid Differentiation of Hematopoietic Stem Cells and Improves Cognition in Aged Mice by Binding to the S100 Calcium-Binding Protein A8 [lenti-A8 RNA-seq]

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Adropin correlates with aging-related neuropathology in humans and improves cognitive function in aging mice.

Project description:The neural functions of adropin, a secreted peptide highly expressed in the brain, have not been investigated. In humans, adropin is highly expressed in astrocytes and peaks during critical postnatal periods of brain development. Gene enrichment analysis of transcripts correlating with adropin expression suggests processes relevant to aging-related neurodegenerative diseases that vary with age and dementia state, possibly indicating survivor bias. In people aged <40 y and 'old-old' (>75 y) diagnosed with dementia, adropin correlates positively with genes involved in mitochondrial processes. In the 'old-old' without dementia adropin expression correlates positively with morphogenesis and synapse function. Potent neurotrophic responses in primary cultured neurons are consistent with adropin supporting the development and function of neural networks. Adropin expression in the 'old-old' also correlates positively with protein markers of tau-related neuropathologies and inflammation, particularly in those without dementia. How variation in brain adropin expression affects neurological aging was investigated using old (18-month) C57BL/6J mice. In mice adropin is expressed in neurons, oligodendrocyte progenitor cells, oligodendrocytes, and microglia and shows correlative relationships with groups of genes involved in neurodegeneration and cellular metabolism. Increasing adropin expression using transgenesis improved spatial learning and memory, novel object recognition, resilience to exposure to new environments, and reduced mRNA markers of inflammation in old mice. Treatment with synthetic adropin peptide also reversed age-related declines in cognitive functions and affected expression of genes involved in morphogenesis and cellular metabolism. Collectively, these results establish a link between adropin expression and neural energy metabolism and indicate a potential therapy against neurological aging.

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