Hyperthermic preconditioning severely accelerates neuronal damage in the gerbil ischemic hippocampal dentate gyrus via decreasing SODs expressions.

Abstract

It is well known that neurons in the dentate gyrus (DG) of the hippocampus are resistant to short period of ischemia. Hyperthermia is a proven risk factor for cerebral ischemia and can produce more extensive brain damage related with mortality rates. The aim of this study was to examine the effect of hyperthermic conditioning (H) on neuronal death, gliosis and expressions of SODs as anti-oxidative enzymes in the gerbil DG following 5 min-transient cerebral ischemia. The animals were randomly assigned to 4 groups: 1) (N+sham)-group was given sham-operation with normothermia (N); 2) (N+ischemia)-group was given 5 min-transient ischemia with N; 3) (H+sham)-group was given sham-operation with H; and 4) (H+ischemia)-group was given 5 min-transient cerebral ischemia with H. H (39±0.5°C) was induced by subjecting the animals to a heating pad for 30 min before and during the operation. In the (N+ischemia)-groups, a significant neuronal death was observed in the polymorphic layer (PL) from 1 day after ischemia-reperfusion. In the (H+ischemia)-groups, neuronal death was also observed in the PL from 1day post-ischemia; the degree of the neuronal death was severer than that in the (N+ischemia)-groups. In addition, we examined the gliosis of astrocytes and microglia using anti-glial fibrillary acidic protein (GFAP) and anti- ionized calcium-binding adapter molecule 1 (Iba-1). GFAP(+) and Iba-1(+) glial cells were much more activated in the (H+ischemia)-groups than those in the (N+ischemia)-groups. On the other hand, immunoreactivities and levels of SOD1 rather than SOD2 were significantly lower in the (H+ischemia)-groups than those in the (N+ischemia)-groups. In brief, on the basis of our findings, we suggest that cerebral ischemic insult with hyperthermic conditioning brings up severer neuronal damage and gliosis in the polymorphic layer through reducing SOD1 expression rather than SOD2 expression in the DG.

• Authors: Dong Won Kim, Jeong-Hwi Cho, Geum-Sil Cho, In Hye Kim, Joon Ha Park, Ji Hyeon Ahn, Bai Hui Chen, Bich-Na Shin, Hyun-Jin Tae, Seongkweon Hong, Jun Hwi Cho, Young-Myeong Kim, Moo-Ho Won, Jae-Chul Lee
• Journal: Journal of the neurological sciences (J Neurol Sci) Vol. 358 Issue 1-2 Pg. 266-75 (Nov 15 2015) ISSN: 1878-5883 [Electronic] Netherlands
• PMID: 26365286 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
• Copyright: Copyright © 2015 Elsevier B.V. All rights reserved.

Chemical References

• Superoxide Dismutase
• Superoxide Dismutase-1
• superoxide dismutase 2

Topics

• Animals
• Astrocytes (metabolism)
• Cell Death
• Dentate Gyrus (pathology)
• Disease Models, Animal
• Fever (pathology)
• Gerbillinae
• Gliosis (etiology, pathology)
• Ischemic Attack, Transient (pathology)
• Male
• Microglia (metabolism)
• Neurons (pathology)
• Reperfusion Injury (pathology)
• Superoxide Dismutase (metabolism)
• Superoxide Dismutase-1