Activation of α7 nicotinic acetylcholine receptor alleviates cerebral cortical neuron injury induced by oxygen- glucose deprivation
10.3724/SP.J.1008.2015.00472
- Author:
Rujuan XIN
1
Author Information
1. Department of Pharmacology, School of Pharmacy, Second Military Medical University
- Publication Type:Journal Article
- Keywords:
Cerebral cortical neurons;
Oxidative stress;
Oxygen-glucose deprivation;
α7 nicotinic acetylcholine receptor
- From:
Academic Journal of Second Military Medical University
2015;36(5):472-476
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect of activatinga7 nicotinic acetylcholine receptor (α7nAchR) on cerebral cortical neurons injury induced by oxygen-glucose deprivation (OGD) and the possible mechanism. Methods Cerebral cortical neurons cultured for 7 d were randomly divided into three groups; control group, OGD group (Cells experienced a 12 h oxygen- glucose deprivation) and OGD group treated with PNU-282987 (Cells experienced a 12 h oxygen-glucose deprivation with PNU- 282987 pretreatment for 24 h). Cell viability was determined by CCK-8 assay, lactate dehydrogenase (LDH) was examined to reflect cell injury, apoptosis and reactive oxygen species (ROS) production were analyzed by flow cytometry, and expression of hemeoxygenase-1 (HO-1) and hypoxia inducible factor-1a (HIF-1a) were detected by Western blotting analysis. Results OGD resulted in cell death, LDH increase, and cell apoptosis. Compared with the OGD group, PNU-282987 pretreated group had significantly increased cell survival (P < 0. 05), significantly decreased LDH level and ROS production (P < 0. 05), and significantly inhibited cell apoptosis (P<0. 05). Meanwhile, HO-1 protein expression was significantly increased and HIF-1α protein expression was significantly reduced in PNU-282987 pretreated group compared with the OGD group (P<0. 05). Conclusion Activation ofα7nAchR can protect cerebral cortical neurons against OGD-induced injury, which may be related to the anti-oxidative stress.
