Expression and function of autophagy after ischemia/reperfusion in rats hippocampus neuron.
- Author:
Fang SU
1
;
Pei ZHANG
;
Zhi-Wei JIANG
;
De-Qing PENG
;
Lu-Ying GAO
;
Shu-Qin LIU
;
Ling-Bo QIAN
;
Zhi-Guo YE
;
Qiang XIA
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Autophagy; physiology; Brain Ischemia; pathology; Cell Hypoxia; Culture Media, Serum-Free; Hippocampus; cytology; pathology; Male; Neurons; pathology; Primary Cell Culture; Rats; Rats, Sprague-Dawley; Reperfusion Injury; pathology
- From: Chinese Journal of Applied Physiology 2011;27(2):187-191
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo explore the expression of autophagy after ischemia/reperfusion and its possible function in rats hippocampus neurons.
METHODSAfter 2 hours oxygen-glucose deprivation and different periods time of reperfusion (OGD/R) treatment in primary hippocampal neurons, neuron viability was evaluated by MTT assay, specific structure of autophagosome and specific protein of autophagy microtubule-associated protein 1 light chain 3 B (LC3B) were detected by transmission electron microscope and immunofluorescence respectively. The inhibitor of autophagy 3-Methyladenine (3-MA) was also used to exam the viability of neurons.
RESULTSTreatment by OGD/R markedly reduced neuronal viability. Compared to the control group, autophagy existed in different time periods after OGD/R shown both in transmission electron microscope and immunofluorescence. Application of 3-MA significantly reduced neuronal viability.
CONCLUSIONOxygen-glucose deprivation can activate autophagy in rat hippocampus neurons, which may resist the injury during ischemia/reperfusion.
