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With the growing population, aging, extended lifespans and anti‑aging have become popular areas of research in the life and social sciences. With increasing age, the structure and function of the testes, the spermatogenetic and androgen‑producing organ in the male reproductive system, gradually declines. Ginsenoside Rg1 is an extract of Panax ginseng in traditional Chinese medicine. The extract facilitates anti‑aging through its anti‑inflammatory and antioxidant properties. However, it has not been reported whether ginsenoside Rg1 delays testicular aging. The present study established D‑galactose (D‑gal)‑induced aging mouse models to examine the protective effects of ginsenoside Rg1 on the structure and function of the testes, and the underlying mechanism. A total of 60 healthy specific pathogen‑free male C57BL/6 mice were randomly divided into four groups: Control group; Rg1 group; D‑gal + Rg1 group; and D‑gal group. The tissues of the mice were used for further experiments. The present study further investigated the effects of Rg1 on the volume of serum testosterone, the testicular index, testicular microscopic structures, the senescence of spermatogenetic cells, the apoptosis of spermatogenetic cells, the activity of the antioxidant enzymes, the levels of inflammatory cytokines, and the levels of S‑phase kinase‑associated protein (p19), cyclin‑dependent kinase inhibitor 1 (p21) and cellular tumor antigen p53 (p53) in D‑gal‑induced aging mice. In general, compared with the D‑gal group, the treatment of Rg1 increased the testis index, serum testosterone level and the active content of superoxide dismutase and the total antioxidant capacity. The percentage of senescence‑associated β‑galactosidase‑positive cells, the level of apoptosis and the volume of methane dicarboxylic aldehyde, tumor necrosis factor‑α, interleukin (IL)‑1β and IL‑6 in testicular tissues were significantly decreased, and the expression of p19, p53 and p21 was downregulated due to the treatment with Rg1. The results of the present study demonstrated that ginsenoside Rg1 was able to protect the testes against D‑gal‑induced aging in mice. In addition, the protective effect of Rg1 may be achieved via antioxidation and downregulation of the p19/p53/p21 signaling pathway. [ABSTRACT FROM AUTHOR]

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., Competing Interests: The authors declare that they have no conflicts of interest., (Copyright © 2019 Yue Xiang et al.)