ERKl/2 signaling pathway mediates heme oxygenase-1 up-regulation by minocycline in PC12 cells exposed to oxygen glucose deprivation.
- Author:
Tao TAO
1
;
Xin-Yue QIN
;
Xun-Tai MA
;
Hua LUO
;
Xiao-Gang LI
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Brain Ischemia; Cell Hypoxia; Cell Survival; Glucose; Heme Oxygenase (Decyclizing); metabolism; MAP Kinase Signaling System; Minocycline; pharmacology; Oxygen; PC12 Cells; Rats; Up-Regulation
- From: Journal of Southern Medical University 2015;35(1):117-120
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effects of minocycline in promoting the survival of pheochromocytoma (PCI2) cells exposed to oxygen glucose deprivation (OGD) and explore the underlying mechanisms.
METHODSAn in vitro cell model of cerebral ischemia was established by OGD for 6 h in PCI2 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-I (HO-I) and phospholylated extracellular signal-regulated protein kinase 1/2 (ERK1/2) by Western blotting.
RESULTSThe cell viability decreased dramatically following OGD. Pretreatment with minocycline (O.I-IO JJ.mol/L) induced a significant increase in the cell viability after OGD and caused up-regulation of HO-I protein and enhanced ERK1/2 phospholylation, and the effects were especially obvious with 1 JJ.mol/L minocycline and were abolished by inhibition of ERK1/2 activity with UOI26 (IO JJ.mol/L).
CONCLUSIONMinocycline can protect PCI2 cells against OGD-induced toxicity by up-regulating HO-I protein expression through ERKl/2 signaling pathways.
