Protective effect of icaritin on apoptosis of primarily cultured rat neurons induced by Abeta25-35 peptide.
- Author:
Xiang-nan ZHANG
1
;
Huan-huan WANG
;
Zhi-qiang WANG
Author Information
- Publication Type:Journal Article
- MeSH: Amyloid beta-Peptides; toxicity; Animals; Apoptosis; drug effects; Cell Survival; drug effects; Cells, Cultured; Cerebral Cortex; cytology; embryology; Drugs, Chinese Herbal; pharmacology; Flavonoids; pharmacology; Neurons; cytology; drug effects; Neuroprotective Agents; pharmacology; Rats; Rats, Sprague-Dawley
- From: Journal of Zhejiang University. Medical sciences 2007;36(3):224-228
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the protective effects of icaritin (ICT) on apoptosis of primarily cultured rat neurons induced by Abeta(25-35) peptide and its mechanism.
METHODSCortical neurons from rat embryonic cortical on d17 pregnancy were cultured in neural basal medium for 7 days. Icaritin (ICT) was pre-incubated for 24 h before adding Abeta(25-35) peptide and then the cells were incubated for 72 h. Neuroprotective effects of ICT were evaluated by MTT assay, LDH level in medium and cell morphological observation. Meanwhile, apoptosis was determined by JC-1 staining for mitochondria membrane potential (DeltaPsim) and AO/EB double staining for genetic damage of nucleoli in monolayer cells.
RESULTS0.1 micromol.L(-1) ICT pre-incubation for 24 h prevented rat neurons from Abeta(25-35) peptide induced apoptosis significantly as demonstrated by MTT, LDH assay and morphological observation. AO/EB double staining also indicated that ICT prevented neurons from apoptosis. JC-1 staining further showed that ICT prevented decreasing of mitochondrial DeltaPsim induced by Abeta(25-35) peptide.
CONCLUSIONICT could protect primarily cultured rat neurons from Abeta(25-35) peptide induced apoptosis.
