Abstract
This is a study on the relationship between the protective effect of ginsenoside Rg1 on senescent neural stem cells and Wnt-β/catenin signaling pathway. Background. Recent studies have shown that overactivation of the Wnt/β-catenin signaling pathway is closely related to stem cell senescence. Whether Rg1 delays the senescence of NSCs is related to the regulation of this signaling pathway. Methods. The whole brain of Nestin-GFP transgenic newborn rat was extracted, and NSCs were extracted and cultured to P3 generation. The following indicators were detected: (1) NSC culture identification, (2) the effect of LiCl on the proliferation and survival rate of NSCs, (3) the effect of ginsenoside Rg1 on the proliferation and survival of NSCs, (4) the growth of NSCs in each group observed by an optical microscope, (5) the cell cycle of each group detected by flow cytometry, (6) the proliferative ability of each group detected by BrdU, (7) the fluorescence intensity of Nestin and Sox2 of NSCs in each group observed by a fluorescence microscope, (8) the positive rate of senescence staining analyzed by SA-β-Gal staining, (9) the localization of β-catenin in NSCs observed by laser confocal microscopy, and (10) the changes of the Wnt/β-catenin pathway-related proteins in each group detected by Western blotting. Results. LiCl activates the Wnt/β-catenin pathway and promotes mouse neural stem cell senescence. Ginsenoside Rg1 promotes proliferation of neural stem cells and inhibits Wnt/β-catenin pathway activation. Conclusions. LiCl can activate the Wnt/β-catenin signaling pathway of NSCs, and ginsenoside Rg1 can antagonize the senescence of NSCs caused by activation of the Wnt/β-catenin signaling pathway and delay brain aging.
Highlights
With the development of modern science and technology, it has been found that stem cells are not “undead” cells
After double labeling with Sox2 protein, the cytoplasmic portion of neural stem cells under the fluorescence microscope was stained with Nestin green fluorescence, and the nucleus portion showed Sox2 red fluorescence (Figure 1)
Our previous studies have shown that brain degenerative diseases in mice are closely related to oxidative stress-induced neural stem cells (NSCs) senescence and that ginsenoside Rg1 can promote hippocampal neurogenesis, improve neural plasticity, and enhance learning and memory
Summary
With the development of modern science and technology, it has been found that stem cells are not “undead” cells. Their self-renewal and multidifferentiation abilities will gradually decline. Many tissues show a decline in regenerative potential coupled with a loss of stem cell function. This will lead to the development of related diseases [1,2,3,4]. The regeneration ability of neural stem cells gradually declines, leading to degeneration and dysfunction of the brain tissue, and eventually causes many degenerative diseases of the central nervous system, such as Parkinson’s disease and Alzheimer’s disease [9, 10]
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