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New insight into Ginseng root polysaccharide GRP-E1F2 on prodynorphin inhibition to delay senescence-associated neuroaging via modulating cellular senescence

ABSTRACT: New insight into Ginseng root polysaccharide GRP-E1F2 on prodynorphin inhibition to delay senescence-associated neuroaging via modulating cellular senescence

PROVIDER: PRJNA1146137 | ENA |

REPOSITORIES: ENA

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Project description:Neuroaging is one of the most distinct signs of aging, which promotes mild cognitive impairment (MCI) and various neurodegenerative diseases. Previous studies have indicated that Panax ginseng C. A. Mey. (ginseng) root polysaccharides have positive effects against senescence and nerve damage. However, its structure and role in delaying senescence-associated neuroaging have not been comprehensively studied. Therefore, this research characterized the structural features of a ginseng root polysaccharide (GRP-E1F2) and the potential mechanism underlying its anti-neurodegeneration effect against senescence-related function and pathological damage. GRP-E1F2 is a neutral polysaccharide with 11.688 kDa molecular weight, which was isolated from the ginseng roots. In this study, NMR, HPLC, FT-IR, and methylation analyses were performed to identify the physiochemical characteristics of GRP-E1F2, which provided its repetitive unit structures. The in vivo experiments revealed that GRP-E1F2 prolonged the lifespan and mitigated senescence-related symptoms including aggregation of lipofuscin and ROS, as well as the antioxidant enzyme inactivation in aging animals (C. elegans and mice). Furthermore, tert-butyl hydroperoxide (tBHP) induced senescent cells indicated that GRP-E1F2 treated has beneficial anti-aging effects. Moreover, the transgenic C. elegans expressing GFP in D-type gamma-aminobutyric acid (GABA)-positive neurons and mice indicated that GRP-E1F2 reduced neuronal morphological abnormalities and reversed aging-induced cognitive deficits, indicating the anti-neuroaging effects of GRP-E1F2. Mechanistically, GRP-E1F2 downregulates cellular senescence in aging brains and cell models, which was indicated by senescence-associated β-galactosidase (SA-β-gal) activity, marker protein p53, p21, phospho-histone H2A.X, and senescence-associated secretory phenotype (SASP). In addition, RNA-seq, RT-qPCR, and immunofluorescence assays revealed that GRP-E1F2 down-regulated mRNA and protein levels of prodynorphin (Pdyn) in aging models. Moreover, the p53 activator and overexpression vectors of Pdyn were employed to determine the pharmacological mechanism of GRP-E1F2 in reducing Pdyn expressions to delay neuroaging by inhibiting the cellular senescence signaling pathway. This research provides theoretical support and experimental evidence for the clinical application of ginseng root polysaccharides against senescence-associated neuroaging, promoting the modern development of traditional medicines from natural polysaccharides.

Project description:Plant productivity is adversely affected by exposure to abiotic stresses including salinity. Leaf tissue undergoes accelerated senescence with exposure to salt stress conditions, culminating in lowered efficiency of photosynthetic machinery. The N6-adenine derivative phytohormone Cytokinin (CK) is well known to delay natural leaf senescence by maintaining functioning photosynthesis processes. How various forms of CK function to control this activity and alter physiological and molecular responses under salt-induced leaf senescence is still not known. Here the CKs, trans-Zeatin (tZ) and its N-glucosylated (tZNGs) forms; tZ7G and tZ9G, were tested for their ability to delay leaf senescence in Arabidopsis thaliana. A modified dark-induced leaf senescence CK bioassay was used to study the physiology of photosynthesis performance as well as transcriptome and proteome level changes in detached leaves, across different phases of salt-induced leaf senescence from 2h-72h. Treatments with different CK forms (tZ, tZ7G, and tZ9G) showed that tZNGs can improve PSII efficiency (Fv/Fm) and increase chlorophyll levels compared to salt only treatments, indicating that these CK forms function as active CK forms in delaying senescence. At the transcript level, tZ, tZ7G, and tZ9G revealed differentially expressed genes (DEGs) across both developmental and salt-treated senescence, with tZNGs predominantly altering DEG in the terminal timepoint of salt-treated leaf senescence. Additionally, we found that tZNGs uniquely regulate crucial biological processes (BPs) including CK signaling compared to tZ. Proteome analysis showed that tZNGs and tZ showed similarities in number of differentially abundant proteins (DAPs) trends across senescence timepoints although each of the three forms showing uniquely abundant proteins. GO term analysis for tZNG regulated genes and proteins revel the enrichment of senescence- and chloroplast-related BPs. This study highlights the role of tZNGs as active cytokinin forms towards delaying salt-treated leaf senescence in Arabidopsis at the physiology, transcriptome, and proteome level.

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New insight into Ginseng root polysaccharide GRP-E1F2 on prodynorphin inhibition to delay senescence-associated neuroaging via modulating cellular senescence

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