Effects of folic acid on pERK1/2 expression of neural stem cells from neonatal rats under hypoxia condition in vitro
10.3969/j.issn.1673-8225.2010.06.008
- VernacularTitle:体外缺氧条件下新生鼠神经干细胞pERK1/2表达与叶酸的影响
- Author:
Yang YANG
;
Guowei HUANG
;
Xumei ZHANG
;
Lin ZHAO
;
Qingju YOU
;
Jiajie LIU
- Publication Type:Journal Article
- From:
Chinese Journal of Tissue Engineering Research
2010;14(6):992-995
- CountryChina
- Language:Chinese
-
Abstract:
BACKGROUND: Previous studies have verified that under normal culture of neural stem cells (NSCs), folic acid can accelerate proliferation of NSCs by phosphorylation of mitogen activated protein kinase path activation ERK1/2. OBJECTIVE: To investigate the effect of folic acid on NSC extracellular signal regulatory protein kinase pERK1/2 under hypoxic condition. METHODS: NSCs from Neonatal rats were cultured in vitro by serum-free culture method, and incubated in a flask at 1×10~8/L. Except normal control group, self-made hypoxia equipment was used in the hypoxia model, folic acid deficiency and folic acid supplemented groups at day 3. At 37 ℃, hypoxia culture was conducted in the thermostat for 6 hours. The contents of folic acid were 4 mg/L, 4 mg/L, 0.65 mg/L, 8 mg/L in the four groups. Cells following 6 days were collected to count the density using trypan blue. RT-PCR was utilized to detect pERK1/2 mRNA expression. Western blot assay was employed to determine pERK1/2 protein expression. RESULTS AND CONCLUSION: Compared with the normal control group, the proliferation of NSCs and the expression of ERK1/2mRNA and pERK1/2 protein were decreased significantly in the hypoxia model group. Compared with the hypoxia model group, the proliferation of NSCs and the expression of ERK1/2mRNA and pERK1/2 protein were increased in the folic acid supplemented group, whereas decreased in the folic acid deficiency group. There were significant differences among groups (P < 0.001). Above-described results verified that folic acid supplementation can activate ERK1/2 phosphorylatin and accelerate proliferation of NSCs under hypoxia condition.
