title: Ginsenoside Rg1 attenuates tau phosphorylation in SK-N-SH induced by Aβ-stimulated THP-1 supernatant and the involvement of p38 pathway activation.
abstract: OBJECTIVE
  In the present study we aimed to investigate the neuroprotective effect of ginsenoside Rg1 (GRg1) on neuronal damage examined in an adopted in vitro inflammatory neurodegeneration model and the involvement of p38 MAPK signal pathway.
  
  
  METHODS
  The supernatant from Aβ(1-40)-stimulated THP-1 monocytes was used as culture medium for SK-N-SH neuroblastoma cells which was used as target neuronal cells. The cell viability of SK-N-SH cells was assessed by detecting lactate dehydrogenase (LDH) leakage; the content of pro-inflammatory cytokine was measured by radioimmunoassay; the expressions of tau phosphorylation, p-38 and synaptophysin (SYN) were evaluated by western blot assay. The microtubule associated protein-2 (MAP-2) expression was confirmed by immunostaining.
  
  
  RESULTS
  Our results showed that incubation of the supernatant from Aβ(1-40)-stimulated THP-1 cells with SK-N-SH neuroblastoma cells for 24h significantly increased LDH leakage, tau and p-38 phosphorylation in SK-N-SH cells with increased interleukin (IL)-1β release into the supernatant of THP-1 cells. Pretreatment of THP-1 cells with GRg1 (50, 100 and 150μM) for 30min before Aβ(1-40)-stimulation inhibited THP-1 cell-mediated Aβ neurotoxicity towards SK-N-SH neuroblastoma and also decreased IL-1β release into THP-1 supernatant dose-dependently. An inhibitor of p38 MAPK, SB203580, had the same effect.
  
  
  CONCLUSIONS
  These results suggested that activation of the p38 cell signal pathway may be involved in monocyte-mediated Aβ neurotoxicity towards SK-N-SH cells. Data obtained from this study demonstrated that GRg1 represented a potential treatment strategy for Alzheimer's disease (AD).
authors.affiliation: Department of Neurology, Henan Provincial People's Hospital, Zhengzhou, Henan province, PR China.
authors.forename: Wei
authors.initials: W
authors.lastname: Li
authors.forename: Yanqi
authors.initials: Y
authors.lastname: Chu
authors.forename: Lan
authors.initials: L
authors.lastname: Zhang
authors.forename: Linlin
authors.initials: L
authors.lastname: Yin
authors.forename: Lin
authors.initials: L
authors.lastname: Li
mesh_terms: D016229:Amyloid beta-Peptides / Q000276:immunology*; D002460:Cell Line; D045744:Cell Line, Tumor; D002470:Cell Survival / Q000187:drug effects; D005786:Gene Expression Regulation / Q000187:drug effects; D036145:Ginsenosides / Q000494:pharmacology*; D006801:Humans; D053583:Interleukin-1beta / Q000276:immunology; D008869:Microtubule-Associated Proteins / Q000235:genetics; D009000:Monocytes / Q000187:drug effects / Q000276:immunology*; D009447:Neuroblastoma / Q000276:immunology / Q000378:metabolism; D009474:Neurons / Q000166:cytology / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism; D018696:Neuroprotective Agents / Q000494:pharmacology*; D010766:Phosphorylation / Q000187:drug effects; D015398:Signal Transduction / Q000187:drug effects; D016708:Synaptophysin / Q000235:genetics; D048051:p38 Mitogen-Activated Protein Kinases / Q000276:immunology*; D016875:tau Proteins / Q000276:immunology*
chemical_list: D016229:Amyloid beta-Peptides; D036145:Ginsenosides; D053583:Interleukin-1beta; C489788:MAP2 protein, human; D008869:Microtubule-Associated Proteins; D018696:Neuroprotective Agents; D016708:Synaptophysin; D016875:tau Proteins; D048051:p38 Mitogen-Activated Protein Kinases; C035054:ginsenoside Rg1