Protective effects of ginseng-ginko extracts combination on rat primary cultured neurons induced by Abeta(1-40).
- Author:
Weihong CONG
1
;
Lisong SHENG
;
Yang LI
;
Peng LI
;
Chengren LIN
;
Jianxun LIU
Author Information
- Publication Type:Journal Article
- MeSH: Alzheimer Disease; drug therapy; Amyloid beta-Peptides; pharmacology; Animals; Apoptosis; drug effects; Caspase 3; metabolism; Cell Proliferation; drug effects; Cells, Cultured; Drug Interactions; Drugs, Chinese Herbal; pharmacology; therapeutic use; Female; Gene Expression Regulation, Enzymologic; drug effects; Ginkgo biloba; chemistry; Male; Neurons; cytology; drug effects; metabolism; ultrastructure; Panax; chemistry; Peptide Fragments; pharmacology; Rats; Rats, Sprague-Dawley; Time Factors
- From: China Journal of Chinese Materia Medica 2011;36(7):908-911
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo observe the injury in rat primary cultured neurons induced by Abeta(1-40) and the protective effects of combination of ginseng and ginko extracts.
METHODPrimary neurons were induced by Abeta(1-40) to establish the cell model of toxic injury. Using flow cytometry with Annexin V-FITC/PI double staining, MTP assay, transmission electron microscopy and Western blot, the appropriate concentration and duration of AP for cell model establishment were determined. The effects of extracts of ginseng and ginko (EGGB)on cellular proliferative activity, apoptotic rate, ultrastructure and caspase-3 expression were detected.
RESULTThe apoptotic rate was increased significantly after neurons were induced by 1 micromol x L(-1) Abeta(-40) for 24 h (P < 0.01). EGGB (5, 50 mg L(-1)) significantly enhanced the proliferative activity (P < 0.05). Meanwhile, EGGB (50 mg L(-1)) inhibited neuronal apoptosis and caspase-3 overexpression and improved cellular ultrastructure remarkably (P < 0.05, P < 0.01).
CONCLUSIONAbeta(1-40) could significantly induce primary cultured neurons to apoptosis in vitro. EGGB showed beneficial neuroprotective effects against neuronal apoptosis, which might be due to improving the structures of neuron and its subcellular organelles, enhancing cellular proliferative activity and inhibiting caspase-3 overexpression in neurons.
