Protective effect of Na2SeO3 against cerebral ischemia-reperfusion injury to the hippocampal neurons in rats.
- Author:
Guang-sheng WANG
1
;
De-qin GENG
;
Yuang-wei WANG
;
Xiao-dong CHEN
;
Tong-hui YANG
;
Chun-hong CHANG
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Apoptosis; Brain Ischemia; metabolism; pathology; Hippocampus; cytology; metabolism; pathology; Interleukin-1beta; metabolism; Male; Nerve Growth Factor; metabolism; Neurons; drug effects; metabolism; pathology; Rats; Rats, Sprague-Dawley; Reperfusion Injury; metabolism; pathology; Sodium Selenite; pharmacology; Tumor Necrosis Factor-alpha; metabolism
- From: Journal of Southern Medical University 2010;30(10):2336-2339
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the protective effects of selenium on rat hippocampal neurons against ischemia-reperfusion (IR) injury.
METHODSThirty-two rats were randomly divided into sham-operated group, IR group and selenium-treated group, and in the latter two groups, cerebral IR injury was induced by middle cerebral artery occlusion; Na2SeO3 treatment was administer in selenium-treated group. At 14 days after reperfusion, the brain tissues were harvested from the rats and hippocampal neuron injuries were observed by TUNEL and Methylene Blue staining. The levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and nerve growth factor (NGF) in the hippocampal tissues were measured by ELISA.
RESULTSCompared with IR group, the rats in selenium-treated group showed no significant increase in the expression of m-NGF (P>0.05), but pro-NGF expression was significantly increased (P<0.05) in the hippocampal tissue. Na2SeO3 treatment significantly inhibited the expressions of TNF-α and IL-1β and decreased the apoptosis of hippocampal neurons following cerebral IR injury (P<0.05).
CONCLUSIONSelenium produces antiapoptotic effect to protect the hippocampal neurons following cerebral IR injury possibly not by increasing the level of m-NGF but by decreasing the expressions of the inflammatory factors.
