Effect of Melatonin on the Changes of Hippocampal Polyamine Content and Neuronal Damage Following Transient Global Ischemia in Mongolian Gerbil: a Study of the Differences of Pre- and Post-ischemic Treatment.
10.4097/kjae.2001.40.5.664
- Author:
Seong Ryong LEE
1
;
Jae Kyu CHEUN
Author Information
1. Departments of Pharmacology, School of Medicine, Keimyung University, Daegu, Korea.
- Publication Type:Original Article
- Keywords:
Brain: global ischemia;
Equipment: high performance liquid chromatography;
rotary microtome;
Pharmacology: melatonin;
polyamine
- MeSH:
Animals;
Carotid Artery, Common;
Chromatography, Liquid;
Eosine Yellowish-(YS);
Gerbillinae*;
Humans;
Ischemia*;
Male;
Melatonin*;
Neurons*;
Neuroprotective Agents;
Putrescine;
Research Personnel;
Spermidine;
Spermine
- From:Korean Journal of Anesthesiology
2001;40(5):664-670
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: We designed this study to examine whether melatonin has a neuroprotective effect against hippocampal neuronal damage following transient global ischemia in a gerbil. Because polyamine is known to participate in the process of ischemic neuronal damage, we examined the influence of melatonin on the polyamine level as well as histology. In particular, we examined the difference between pre- and post-ischemic treatments of melatonin by using the above mentioned parameters. METHODS: Male Mongolian gerbils (60 - 80 g) were used in this study. Transient global ischemia was induced by occlusion of the bilateral common carotid arteries for 3 min with microclips. Melatonin was administered 1 h before or 1 h after occlusion. The animals were dissected 4 days after the occlusion for polyamine measurement by a high performance liquid chromatography (HPLC) and histological evaluation (hematoxylin and eosin staining). A histological examination was performed by a blinded investigator. RESULTS: The hippocampal putrescine (PU) level increased compared to sham-operated animals and the increase of PU was attenuated by melatonin administration (pre- or post-ischemic treatment). Spermidine (SD) and spermine (SM) levels didn't show significant changes after ischemia. Hippocampal neuronal damage in the CA1 region was markedly observed in vehicle-treated animals compared to sham- operated animals. Both pre- and post-ischemic melatonin administration significantly inhibited hippocampal CA1 neuronal damage compared to corresponding vehicle-treated animals (P < 0.01, respectively). CONCLUSIONS: Melatonin attenuates the polyamine response following transient global ischemia and may have putative neuroprotective effects against global ischemia-induced neuronal damage. There is no difference in neuroprotective effects of melatonin between pre- & post-ischemic treatments.
