Role of PI3K/Akt pathway in effect of paeoniflorin against Aβ25-35-induced PC12 cell injury.
- Author:
Ling LIU
;
Shu-Ying WANG
;
Jian-Gang WANG
- Publication Type:Journal Article
- MeSH: Alzheimer Disease; drug therapy; genetics; metabolism; physiopathology; Amyloid beta-Peptides; toxicity; Animals; Apoptosis; drug effects; Cell Survival; drug effects; Drugs, Chinese Herbal; pharmacology; Glucosides; pharmacology; Humans; Monoterpenes; pharmacology; Neurons; cytology; drug effects; metabolism; Neuroprotective Agents; pharmacology; PC12 Cells; Peptide Fragments; toxicity; Phosphatidylinositol 3-Kinases; genetics; metabolism; Proto-Oncogene Proteins c-akt; genetics; metabolism; Proto-Oncogene Proteins c-bcl-2; genetics; metabolism; Rats; Signal Transduction; drug effects
- From: China Journal of Chinese Materia Medica 2014;39(20):4045-4049
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo study the role of PI3K/Akt pathway in the neuroprotective effect of paeoniflorin on PC12 cells.
METHODThe paeoniflorin group (5, 10, 20 μmol · L(-1)) was pretreated for 30 min, and then added with Aβ25-35 (20 μmol · L(-1)) for interaction for 24 h. Inhibitor LY294002 (10 μmol · L(-1)) was pretreated for 30 min before the action of paeoniflorin (10 μmol · L(-1)). The MTT colorimetric method was used to detect the cell viability. The apoptosis rate was tested by the FITC-Annexin V/PI staining. The protein expression of p-AKT, Bax, Bcl-2 and cleaved caspase-3 protein were detected by Western blot analysis.
RESULTPaeoniflorin could significantly inhibit the Aβ25-35-induced PC12 cell toxicity and apoptosis. Its protection effect may be achieved by up- regulating AKT phosphorylation level, increasing Bcl-2 protein expression, reducing Bax protein expression, inhibiting the activation of caspase-3. Inhibitor LY294002 could weaken the above protective effects of paeoniflorin.
CONCLUSIONPaeoniflorin could activate PI3K/Akt signaling pathway to protect the PC12 cell injury induced by Aβ25-35.