[Correlation between induction of ischemic tolerance and expression of heat shock protein-70 in the rat hippocampus].
We investigated the correlation between protection against ischemic neuronal damage by preconditioning with sublethal ischemia and the expression of heat shock protein-70 (HSP70). Three minutes of forebrain ischemia in the rat induced by four-vessel occlusion and 3 days of reperfusion was followed by 6, 8, and 10 minutes of ischemia. Seven days after the second ischemia, the brains were used for histology. Two hours, 1, 3, and 7 days after 3 or 6 minutes of ischemia, the brains were used for immunohistochemistry with an antibody raised against HSP70. Three minutes of ischemia produced no neuronal damage in the hippocampus. Six, 8, and 10 minutes of ischemia produced severe neuronal damage to CA1. However, CA1 neurons were preserved in animals subjected to 6 and 8 minutes of ischemia following preconditioning with 3 minutes of ischemia. Immunostaining showed that HSP70 was induced in the CA1 subfield 3 days after 3 minutes of ischemia. HSP70 was stained in the CA1, CA3, and CA4 subfields 1 and 3 days after 6 minutes of ischemia with or without preconditioning. However, HSP70 was also stained in CA1 2 hours and 7 days after 6 minutes of ischemia following preconditioning. These results strongly suggest that stress response induced by sublethal ischemia protects against ischemic neuronal damage. However, the protection was not seen when HSP70 synthesis was delayed. Presence of HSP70 during and immediately after ischemia may be critical for the protection against ischemic neuronal damage following preconditioning.
Liu
Y
Y
Department of Neurology, Tohoku University School of Medicine, Sendai, Japan.
Kato
H
H
Nakata
N
N
Kogure
K
K
D000818:Animals; D002545:Brain Ischemia / Q000473:pathology / Q000503:physiopathology*; D006360:Heat-Shock Proteins / Q000502:physiology*; D006624:Hippocampus / Q000473:pathology; D008297:Male; D051381:Rats; D017208:Rats, Wistar
D006360:Heat-Shock Proteins