Tags

Type your tag names separated by a space and hit enter

Ginsenoside Rg1 Decreases Oxidative Stress and Down-Regulates Akt/mTOR Signalling to Attenuate Cognitive Impairment in Mice and Senescence of Neural Stem Cells Induced by D-Galactose.
Neurochem Res. 2018 Feb; 43(2):430-440.NR

Abstract

Adult hippocampal neurogenesis plays a pivotal role in learning and memory. The suppression of hippocampal neurogenesis induced by an increase of oxidative stress is closely related to cognitive impairment. Neural stem cells which persist in the adult vertebrate brain keep up the production of neurons over the lifespan. The balance between pro-oxidants and anti-oxidants is important for function and surviving of neural stem cells. Ginsenoside Rg1 is one of the most active components of Panax ginseng, and many studies suggest that ginsenosides have antioxidant properties. This research explored the effects and underlying mechanisms of ginsenoside Rg1 on protecting neural stem cells (NSCs) from oxidative stress. The sub-acute ageing of C57BL/6 mice was induced by subcutaneous injection of D-gal (120 mg kg-1 day-1) for 42 day. On the 14th day of D-gal injection, the mice were treated with ginsenoside Rg1 (20 mg kg-1 day-1, intraperitoneally) or normal saline for 28 days. The study monitored the effects of Rg1 on proliferation, senescence-associated and oxidative stress biomarkers, and Akt/mTOR signalling pathway in NSCs. Compared with the D-gal group, Rg1 improved cognitive impairment induced by D-galactose in mice by attenuating senescence of neural stem cells. Rg1 also decreased the level of oxidative stress, with increased the activity of superoxide dismutase and glutathione peroxidase in vivo and in vitro. Rg1 furthermore reduced the phosphorylation levels of protein kinase B (Akt) and the mechanistic target of rapamycin (mTOR) and down-regulated the levels of downstream p53, p16, p21 and Rb in D-gal treated NSCs. The results suggested that the protective effect of ginsenoside Rg1 on attenuating cognitive impairment in mice and senescence of NSCs induced by D-gal might be related to the reduction of oxidative stress and the down-regulation of Akt/mTOR signaling pathway.

Authors+Show Affiliations

Laboratory of Stem Cells and Tissue Engineering, Chongqing Medical University, Chongqing, China.Laboratory of Stem Cells and Tissue Engineering, Chongqing Medical University, Chongqing, China.Laboratory of Stem Cells and Tissue Engineering, Chongqing Medical University, Chongqing, China.Laboratory of Stem Cells and Tissue Engineering, Chongqing Medical University, Chongqing, China.Laboratory of Stem Cells and Tissue Engineering, Chongqing Medical University, Chongqing, China.Laboratory of Stem Cells and Tissue Engineering, Chongqing Medical University, Chongqing, China.Laboratory of Stem Cells and Tissue Engineering, Chongqing Medical University, Chongqing, China.Laboratory of Stem Cells and Tissue Engineering, Chongqing Medical University, Chongqing, China. ypwangcq@aliyun.com. Department of Histology and Embryology, Chongqing Medical University, 1 Yixueyuan Road, Yuzhong District, Chongqing, 400016, China. ypwangcq@aliyun.com.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

29147958

Citation

Chen, Linbo, et al. "Ginsenoside Rg1 Decreases Oxidative Stress and Down-Regulates Akt/mTOR Signalling to Attenuate Cognitive Impairment in Mice and Senescence of Neural Stem Cells Induced By D-Galactose." Neurochemical Research, vol. 43, no. 2, 2018, pp. 430-440.
Chen L, Yao H, Chen X, et al. Ginsenoside Rg1 Decreases Oxidative Stress and Down-Regulates Akt/mTOR Signalling to Attenuate Cognitive Impairment in Mice and Senescence of Neural Stem Cells Induced by D-Galactose. Neurochem Res. 2018;43(2):430-440.
Chen, L., Yao, H., Chen, X., Wang, Z., Xiang, Y., Xia, J., Liu, Y., & Wang, Y. (2018). Ginsenoside Rg1 Decreases Oxidative Stress and Down-Regulates Akt/mTOR Signalling to Attenuate Cognitive Impairment in Mice and Senescence of Neural Stem Cells Induced by D-Galactose. Neurochemical Research, 43(2), 430-440. https://doi.org/10.1007/s11064-017-2438-y
Chen L, et al. Ginsenoside Rg1 Decreases Oxidative Stress and Down-Regulates Akt/mTOR Signalling to Attenuate Cognitive Impairment in Mice and Senescence of Neural Stem Cells Induced By D-Galactose. Neurochem Res. 2018;43(2):430-440. PubMed PMID: 29147958.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Ginsenoside Rg1 Decreases Oxidative Stress and Down-Regulates Akt/mTOR Signalling to Attenuate Cognitive Impairment in Mice and Senescence of Neural Stem Cells Induced by D-Galactose. AU - Chen,Linbo, AU - Yao,Hui, AU - Chen,Xiongbin, AU - Wang,Ziling, AU - Xiang,Yue, AU - Xia,Jieyu, AU - Liu,Ying, AU - Wang,Yaping, Y1 - 2017/11/17/ PY - 2017/06/19/received PY - 2017/11/14/accepted PY - 2017/11/09/revised PY - 2017/11/18/pubmed PY - 2018/8/17/medline PY - 2017/11/18/entrez KW - Ginsenoside Rg1 KW - Neural stem cell KW - Oxidative stress KW - Senescence SP - 430 EP - 440 JF - Neurochemical research JO - Neurochem. Res. VL - 43 IS - 2 N2 - Adult hippocampal neurogenesis plays a pivotal role in learning and memory. The suppression of hippocampal neurogenesis induced by an increase of oxidative stress is closely related to cognitive impairment. Neural stem cells which persist in the adult vertebrate brain keep up the production of neurons over the lifespan. The balance between pro-oxidants and anti-oxidants is important for function and surviving of neural stem cells. Ginsenoside Rg1 is one of the most active components of Panax ginseng, and many studies suggest that ginsenosides have antioxidant properties. This research explored the effects and underlying mechanisms of ginsenoside Rg1 on protecting neural stem cells (NSCs) from oxidative stress. The sub-acute ageing of C57BL/6 mice was induced by subcutaneous injection of D-gal (120 mg kg-1 day-1) for 42 day. On the 14th day of D-gal injection, the mice were treated with ginsenoside Rg1 (20 mg kg-1 day-1, intraperitoneally) or normal saline for 28 days. The study monitored the effects of Rg1 on proliferation, senescence-associated and oxidative stress biomarkers, and Akt/mTOR signalling pathway in NSCs. Compared with the D-gal group, Rg1 improved cognitive impairment induced by D-galactose in mice by attenuating senescence of neural stem cells. Rg1 also decreased the level of oxidative stress, with increased the activity of superoxide dismutase and glutathione peroxidase in vivo and in vitro. Rg1 furthermore reduced the phosphorylation levels of protein kinase B (Akt) and the mechanistic target of rapamycin (mTOR) and down-regulated the levels of downstream p53, p16, p21 and Rb in D-gal treated NSCs. The results suggested that the protective effect of ginsenoside Rg1 on attenuating cognitive impairment in mice and senescence of NSCs induced by D-gal might be related to the reduction of oxidative stress and the down-regulation of Akt/mTOR signaling pathway. SN - 1573-6903 UR - https://www.unboundmedicine.com/medline/citation/29147958/Ginsenoside_Rg1_Decreases_Oxidative_Stress_and_Down_Regulates_Akt/mTOR_Signalling_to_Attenuate_Cognitive_Impairment_in_Mice_and_Senescence_of_Neural_Stem_Cells_Induced_by_D_Galactose_ L2 - https://doi.org/10.1007/s11064-017-2438-y DB - PRIME DP - Unbound Medicine ER -