Post-conditioning exacerbates the MnSOD immune-reactivity after experimental cerebral global ischemia and reperfusion in the rat brain hippocampus.
This study monitored the effects of sub-lethal ischemia (post-conditioning) applied after a previous ischemic attack by way of the MnSOD immune-reactivity examined in CA1 and dentate gyrus of the rat hippocampus. The experimental 10 min transient cerebral ischemia was followed by 2 days of reperfusion, the rats then underwent a second ischemia (4 or 6 min post-conditioning). MnSOD immune-reactivity was evaluated after 5 h, 1 and 2 days. Results obtained by computer microdensitometric image analysis indicated that 4 min of ischemic post-conditioning caused higher MnSOD immune-reactivity than 6 min. However, higher viability of CA1 neurons after stronger (6 min) post-conditioning when production of MnSOD is lower, as well as differences between MnSOD in CA1 and dentate gyrus indicates another mechanism switching pro-apoptotic destination of CA1 neurons to anti-apoptotic.
Nemethova
Miroslava
M
Institute of Neurobiology, Slovak Academy of Sciences, Soltesovej 4-6, 040 01 Kosice, Slovakia. nemeth@saske.sk
Danielisova
Viera
V
Gottlieb
Miroslav
M
Burda
Jozef
J
D000818:Animals; D002545:Brain Ischemia / Q000503:physiopathology*; D006624:Hippocampus / Q000201:enzymology*; D007150:Immunohistochemistry; D019194:Ischemic Preconditioning / Q000379:methods; D008297:Male; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000503:physiopathology*; D013482:Superoxide Dismutase / Q000276:immunology* / Q000378:metabolism
D013482:Superoxide Dismutase