Abstract
Recently, the beneficial role of minocycline on endogenous neurogenesis after cerebral
ischemia has been contradicted by many reports. We examined whether minocycline influences
post-ischemic neurogenesis in the subventricular zone. Adult male Sprague–Dawley rats
were subjected to focal cerebral ischemia for 2 h, and divided into a minocycline-treated
(90 mg/Kg on reperfusion and 45 mg/Kg daily for maintenance) and a saline-treated
group. Bromodeoxyuridine was injected to determine levels of cell proliferation. Inflammation
was assessed by counting polymorphonuclear cell and activated microglia and by measuring
myeloperoxidase activity. Endogenous neurogenesis was quantified by immunohistochemical
staining and functional outcome was measured by infarct size and behavioral tests.
Minocycline treatment decreased inflammation on 1st and 4th days after ischemia. BrdU-positive
cells on 7th day (saline vs. minocycline: 602.80±146.96 vs. 399.40±109.69) and the number of double labeling cells of BrdU/NeuN on 7th day (13.00±4.36 vs. 6.40±2.07) and BrdU/DCx on 4th day (17.00±5.00 vs. 7.50±1.91) were significantly decreased in minocycline-treated rats. Infarct size and behavioral
tests were not different. Our results indicate that minocycline may reduce immediate
post-ischemic neurogenesis despite adequately suppressed inflammation.
Keywords
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Article info
Publication history
Published online: January 30, 2009
Accepted:
December 15,
2008
Received in revised form:
November 18,
2008
Received:
June 24,
2008
Identification
Copyright
© 2009 Elsevier B.V. Published by Elsevier Inc. All rights reserved.