Abstract
We examined the protective activity of 2,6-diisopropylphenol on mortality and delayed hippocampal cell death induced by transient cerebral ischemia in the gerbil. Forebrain ischemia was produced by bilaterally occluding the common carotid arteries for 10 minutes; then the blood supply to the brain was restored. The number of survivors was counted for 8 days, and the histopathological damage in the CA1 region of the hippocampus was scored according to the semiquantitative scale of Rudolphi and Colleagues. When intraperitoneally injected immediately after the ischemic attack, 2,6-diisopropylphenol (25, 50, 100 mg kg-1) produced no significant reduction in the rate of mortality in comparison with its vehicle. However, the survivors that had received the compound at the dose of 50 and 100 mg kg-1 elicited a significant increase in the number of viable pyramidal cells in the CA1hippocampal region. Moreover, we obtained similar results by injecting the compound 30 minutes after the release of the carotid artery occlusion. These results suggest that 2,6-diisopropylphenol, although it does not show any capability of improving the rate of survival, it elicits protective properties against the transient forebrain ischemia-induced delayed hippocampal neuronal death.
| Original language | English |
|---|---|
| Pages (from-to) | 961-970 |
| Number of pages | 10 |
| Journal | Life Sciences |
| Volume | 58 |
| Issue number | 12 |
| DOIs | |
| Publication status | Published - Feb 16 1996 |
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Keywords
- Delayed neuronal death
- Propofol
- Transient forebrain ischemia
ASJC Scopus subject areas
- Pharmacology
Cite this
Effect of 2,6-diisopropylphenol on the delayed hippocampal cell loss following transient forebrain ischemia in the gerbil. / Arcadi, Francesca A.; Rapisarda, Antonio; De Luca, Roberto; Trimarchi, Giuseppe R.; Costa, Giovanni.
In: Life Sciences, Vol. 58, No. 12, 16.02.1996, p. 961-970.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Effect of 2,6-diisopropylphenol on the delayed hippocampal cell loss following transient forebrain ischemia in the gerbil
AU - Arcadi, Francesca A.
AU - Rapisarda, Antonio
AU - De Luca, Roberto
AU - Trimarchi, Giuseppe R.
AU - Costa, Giovanni
PY - 1996/2/16
Y1 - 1996/2/16
N2 - We examined the protective activity of 2,6-diisopropylphenol on mortality and delayed hippocampal cell death induced by transient cerebral ischemia in the gerbil. Forebrain ischemia was produced by bilaterally occluding the common carotid arteries for 10 minutes; then the blood supply to the brain was restored. The number of survivors was counted for 8 days, and the histopathological damage in the CA1 region of the hippocampus was scored according to the semiquantitative scale of Rudolphi and Colleagues. When intraperitoneally injected immediately after the ischemic attack, 2,6-diisopropylphenol (25, 50, 100 mg kg-1) produced no significant reduction in the rate of mortality in comparison with its vehicle. However, the survivors that had received the compound at the dose of 50 and 100 mg kg-1 elicited a significant increase in the number of viable pyramidal cells in the CA1hippocampal region. Moreover, we obtained similar results by injecting the compound 30 minutes after the release of the carotid artery occlusion. These results suggest that 2,6-diisopropylphenol, although it does not show any capability of improving the rate of survival, it elicits protective properties against the transient forebrain ischemia-induced delayed hippocampal neuronal death.
AB - We examined the protective activity of 2,6-diisopropylphenol on mortality and delayed hippocampal cell death induced by transient cerebral ischemia in the gerbil. Forebrain ischemia was produced by bilaterally occluding the common carotid arteries for 10 minutes; then the blood supply to the brain was restored. The number of survivors was counted for 8 days, and the histopathological damage in the CA1 region of the hippocampus was scored according to the semiquantitative scale of Rudolphi and Colleagues. When intraperitoneally injected immediately after the ischemic attack, 2,6-diisopropylphenol (25, 50, 100 mg kg-1) produced no significant reduction in the rate of mortality in comparison with its vehicle. However, the survivors that had received the compound at the dose of 50 and 100 mg kg-1 elicited a significant increase in the number of viable pyramidal cells in the CA1hippocampal region. Moreover, we obtained similar results by injecting the compound 30 minutes after the release of the carotid artery occlusion. These results suggest that 2,6-diisopropylphenol, although it does not show any capability of improving the rate of survival, it elicits protective properties against the transient forebrain ischemia-induced delayed hippocampal neuronal death.
KW - Delayed neuronal death
KW - Propofol
KW - Transient forebrain ischemia
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UR - http://www.scopus.com/inward/citedby.url?scp=0029876962&partnerID=8YFLogxK
U2 - 10.1016/0024-3205(96)00044-6
DO - 10.1016/0024-3205(96)00044-6
M3 - Article
VL - 58
SP - 961
EP - 970
JO - Life Sciences
JF - Life Sciences
SN - 0024-3205
IS - 12
ER -