PMID- 29147958
OWN - NLM
STAT- MEDLINE
DCOM- 20180816
LR  - 20211204
IS  - 1573-6903 (Electronic)
IS  - 0364-3190 (Linking)
VI  - 43
IP  - 2
DP  - 2018 Feb
TI  - 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.
PG  - 430-440
LID - 10.1007/s11064-017-2438-y [doi]
AB  - 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.
FAU - Chen, Linbo
AU  - Chen L
AD  - Laboratory of Stem Cells and Tissue Engineering, Chongqing Medical University, 
      Chongqing, China.
FAU - Yao, Hui
AU  - Yao H
AD  - Laboratory of Stem Cells and Tissue Engineering, Chongqing Medical University, 
      Chongqing, China.
FAU - Chen, Xiongbin
AU  - Chen X
AD  - Laboratory of Stem Cells and Tissue Engineering, Chongqing Medical University, 
      Chongqing, China.
FAU - Wang, Ziling
AU  - Wang Z
AD  - Laboratory of Stem Cells and Tissue Engineering, Chongqing Medical University, 
      Chongqing, China.
FAU - Xiang, Yue
AU  - Xiang Y
AD  - Laboratory of Stem Cells and Tissue Engineering, Chongqing Medical University, 
      Chongqing, China.
FAU - Xia, Jieyu
AU  - Xia J
AD  - Laboratory of Stem Cells and Tissue Engineering, Chongqing Medical University, 
      Chongqing, China.
FAU - Liu, Ying
AU  - Liu Y
AD  - Laboratory of Stem Cells and Tissue Engineering, Chongqing Medical University, 
      Chongqing, China.
FAU - Wang, Yaping
AU  - Wang Y
AD  - Laboratory of Stem Cells and Tissue Engineering, Chongqing Medical University, 
      Chongqing, China. ypwangcq@aliyun.com.
AD  - Department of Histology and Embryology, Chongqing Medical University, 1 Yixueyuan 
      Road, Yuzhong District, Chongqing, 400016, China. ypwangcq@aliyun.com.
LA  - eng
GR  - 30973818/National Natural Science Foundation of China/
GR  - 20125503110006/the Science Foundation of Ministry of Education of China/
PT  - Journal Article
DEP - 20171117
PL  - United States
TA  - Neurochem Res
JT  - Neurochemical research
JID - 7613461
RN  - 0 (Antioxidants)
RN  - 0 (Ginsenosides)
RN  - EC 1.11.1.9 (Glutathione Peroxidase)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
RN  - PJ788634QY (ginsenoside Rg1)
RN  - X2RN3Q8DNE (Galactose)
SB  - IM
MH  - Animals
MH  - Antioxidants/pharmacology
MH  - Cognitive Dysfunction/*drug therapy/metabolism
MH  - Galactose/*pharmacology
MH  - Ginsenosides/*metabolism
MH  - Glutathione Peroxidase/metabolism
MH  - Mice, Inbred C57BL
MH  - Neural Stem Cells/*drug effects
MH  - Oxidative Stress/*drug effects
MH  - Proto-Oncogene Proteins c-akt/drug effects/metabolism
MH  - TOR Serine-Threonine Kinases/metabolism
OTO - NOTNLM
OT  - Ginsenoside Rg1
OT  - Neural stem cell
OT  - Oxidative stress
OT  - Senescence
EDAT- 2017/11/18 06:00
MHDA- 2018/08/17 06:00
CRDT- 2017/11/18 06:00
PHST- 2017/06/19 00:00 [received]
PHST- 2017/11/14 00:00 [accepted]
PHST- 2017/11/09 00:00 [revised]
PHST- 2017/11/18 06:00 [pubmed]
PHST- 2018/08/17 06:00 [medline]
PHST- 2017/11/18 06:00 [entrez]
AID - 10.1007/s11064-017-2438-y [pii]
AID - 10.1007/s11064-017-2438-y [doi]
PST - ppublish
SO  - Neurochem Res. 2018 Feb;43(2):430-440. doi: 10.1007/s11064-017-2438-y. Epub 2017 
      Nov 17.