ERK1/2 signaling pathway mediates heme oxygenase-1 up-regulation by minocycline in PC12 cells exposed to oxygen glucose deprivation
10.3969/j.issn.1673-4254.2015.01.23
- VernacularTitle:ERK1/2通路介导米诺环素促进PC12细胞氧糖剥夺后血红素加氧酶-1的表达
- Author:
Tao TAO
1
;
Xinyue QIN
;
Xuntai MA
;
Hua LUO
;
Xiaogang LI
Author Information
1. 泸州医学院附属医院神经内科
- Keywords:
minocycline;
heme oxygenase-1;
oxygen glucose deprivation;
extracellular signal-regulated kinase 1/2;
PC12 cells
- From:
Journal of Southern Medical University
2015;(1):117-120
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effects of minocycline in promoting the survival of pheochromocytoma (PC12) cells exposed to oxygen glucose deprivation (OGD) and explore the underlying mechanisms. Methods An in vitro cell model of cerebral ischemia was established by OGD for 6 h in PC12 cells with pretreatment with minocycline or an ERK1/2 inhibitor. At 24 h after OGD injury, the cells were evaluated for cell viability by MTT assay and expressions of heme oxygenase-1 (HO-1) and phospholylated extracellular signal-regulated protein kinase 1/2 (ERK1/2) by Western blotting. Results The cell viability decreased dramatically following OGD. Pretreatment with minocycline (0.1-10 μmol/L) induced a significant increase in the cell viability after OGD and caused up-regulation of HO-1 protein and enhanced ERK1/2 phospholylation, and the effects were especially obvious with 1 μmol/L minocycline and were abolished by inhibition of ERK1/2 activity with U0126 (10 μmol/L). Conclusion Minocycline can protect PC12 cells against OGD-induced toxicity by up-regulating HO-1 protein expression through ERK1/2 signaling pathways.
