Effects of alpha-Lipoic Acid on Apoptotic Cell Death in Rat Hippocampus Following Transient Forebrain Ischemia-reperfusion Injury.
- Author:
Hun Cheol AHN
1
;
Jin Ho SONG
;
Kwang Seok KIM
;
Su Jin YOO
Author Information
1. Department of Emergency Medicine, Wonkwang University School of Medicine, Korea. ysoojin@wmc.wonkwang.ac.kr
- Publication Type:Original Article
- Keywords:
Forebrain ischemia-reperfusion injury;
Apoptosis;
alpha-Lipoic acid;
Hippocampus
- MeSH:
Animals;
Apoptosis;
Apoptosis Inducing Factor;
Blotting, Western;
Caspase 3;
Cell Death*;
Hippocampus*;
Ischemia;
Neurons;
Prosencephalon*;
Pyramidal Cells;
Rats*;
Rats, Sprague-Dawley;
Reperfusion Injury*;
RNA, Messenger;
Thioctic Acid*
- From:Journal of the Korean Society of Emergency Medicine
2007;18(2):134-142
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
PURPOSE: The purpose of this study was to evaluate effect of alpha-lipoic acid on apoptotic cell death in rat hippocampal neuron following transient forebrain ischemia-reperfusion (I/R) injury. METHODS: The four-vessel occlusion method was used to induce transient I/R injury in the forebrain of Sprague-Dawley rats. In the treatment group, alpha-Lipoic acid (LA) was administered subcutaneously at 50 mg/kg/day for 7 days before induction of I/R injury. RESULTS: Pretreatment with LA significantly reduced the number of TUNEL-positive neurons in the pyramidal cells layer of the hipocampal CA1 region 5 days after the ischemia, suggesting a marked reduction of apoptotic cell death. Pretreatment with LA also resulted in marked suppression at the transcript level of mRNA for caspase-3 at 24 hours, and decreased concentration of the active form of caspase-3 protein in the hippocampus at 1, 3, and 5 days after I/R injury. Furthermore, as indicated by western blot analysis, the concentration of apoptosis-inducing factor (AIF) in the hippocampus was reduced at 1 and 3 days after a transient I/R injury by pretreatment with LA. CONCLUSION: The results of this study suggest that LA has the potential to prevent neuronal cell death in the hippocampus by inhibiting intracellular signaling pathways responsible for apoptosis following transient I/R injury.
