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1.
Stem Cells Int ; 2019: 5010184, 2019.
Article in English | MEDLINE | ID: mdl-31885611

ABSTRACT

This is a study on the relationship between the protective effect of ginsenoside Rg1 on senescent neural stem cells and Wnt-ß/catenin signaling pathway. Background. Recent studies have shown that overactivation of the Wnt/ß-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-ß-Gal staining, (9) the localization of ß-catenin in NSCs observed by laser confocal microscopy, and (10) the changes of the Wnt/ß-catenin pathway-related proteins in each group detected by Western blotting. Results. LiCl activates the Wnt/ß-catenin pathway and promotes mouse neural stem cell senescence. Ginsenoside Rg1 promotes proliferation of neural stem cells and inhibits Wnt/ß-catenin pathway activation. Conclusions. LiCl can activate the Wnt/ß-catenin signaling pathway of NSCs, and ginsenoside Rg1 can antagonize the senescence of NSCs caused by activation of the Wnt/ß-catenin signaling pathway and delay brain aging.

2.
Zhongguo Zhong Yao Za Zhi ; 39(22): 4442-7, 2014 Nov.
Article in Chinese | MEDLINE | ID: mdl-25850282

ABSTRACT

Neurodegenerative disease is common and frequently occurs in elderly patients. Previous studies have shown that ginsenoside Rg1 was able to inhibit senescent of brain, but the mechanism on the brain during the treatment remains elucidated. To study the mechanism of ginsenoside Rg1 in the process of anti-aging of brain, forty male SD rats were randomly divided into normal group, Rg1 normal group, brain aging model group and Rg1 brain aging model group, each group with 10 rats (brain aging model group: subcutaneous injection of D-galactose (120 mg kg(-1)), qd for 42 consecutive days; Rg1 brain aging model group: while copying the same test as that of brain aging model group, begin intraperitoneal injection of ginsenosides Rg1 (20 mg x kg(-1)) qd for 27 d from 16 d. Rg1 normal group: subcutaneous injection of the same amount of saline; begin intraperitoneal injection of ginsenosides Rg1 (20 mg x kg(-1)) qd for 27 d from 16 d. Normal: injected with an equal volume of saline within the same time. Perform the related experiment on the second day after finishing copying the model or the completion of the first two days of drug injections). Learning and memory abilities were measured by Morris water maze. The number of senescent cells was detected by SA-beta-Gal staining while the level of IL-1 and IL-6 proinflammatory cytokines in hippocampus were detected by ELISA. The activities of SOD, contents of GSH in hippo- campus were quantified by chromatometry. The change of telomerase activities and telomerase length were performed by TRAP-PCR and southern blotting assay, respectively. It is pointed that, in brain aging model group, the spatial learning and memory capacities were weaken, SA-beta-Gal positive granules increased in section of brain tissue, the activity of antioxidant enzyme SOD and the contents of GSH decreased in hippocampus, the level of IL-1 and IL-6 increased in hippocampus, while the length of telomere and the activity of telomerase decreased in hippocampus. Rats of Rg1 brain aging group had their spatial learning and memory capacities enhanced, SA-beta-Gal positive granules in section of brain tissue decreased, the activity of antioxidant enzyme SOD and the contents of GSH increased in hippocampus, the level of IL-1 and IL-6 in hippocampus decreased, the length contraction of telomere suppressed while the change of telomerase activity increased in hippocampus. Compared with that of normal group, the spatial learning and memory capacities were enhanced in Rg1 normal group, SA-beta-Gal positive granules in section of brain tissue decreased in Rg1 normal group, the level of IL-1 and IL-6 in hippocampus decreased in Rg1 normal group. The results indicated that improvement of antioxidant ability, regulating the level of proinflammatory cytokines and regulation of telomerase system may be the underlying anti-aging mechanism of Ginsenoside Rg1.


Subject(s)
Aging/drug effects , Brain/drug effects , Ginsenosides/pharmacology , Animals , Male , Rats , Rats, Sprague-Dawley
3.
Huan Jing Ke Xue ; 29(11): 3124-7, 2008 Nov.
Article in Chinese | MEDLINE | ID: mdl-19186814

ABSTRACT

Aerobic granules were cultivated with synthetic wastewater and were added in the course of aerobic starvation. Results showed that EPS produced by aerobic granules was composed of 40% biodegradable and 60% nonbiodegradable EPS. Among these, only biodegradable EPS could be utilized by their producers, while nonbiodegradable EPS contributed to maintain the spatial structures of aerobic granules. EPS extracted from fresh aerobic granules was fed as the sole carbon source to their own producers and activated sludge and was utilized by them. The average biodegradation rate of activated sludge in terms of EPS was 1.5 times faster than that of aerobic granules. When EPS extracted from starved aerobic granules was fed as the sole carbon source to their own producers and activated sludge, it could not be utilized and could not be energy source.


Subject(s)
Biopolymers/metabolism , Bioreactors , Extracellular Matrix/metabolism , Sewage/chemistry , Waste Disposal, Fluid/methods , Aerobiosis , Biodegradation, Environmental , Biopolymers/chemistry , Extracellular Matrix/chemistry
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