BACKGROUND: Carbon monoxide has been regarded as a gaseous molecular messenger like nitric oxide. PURPOSE: To clarify the role of heme oxygenase-1 in the permanent cerebral ischemia at the protein and mRNA level. METHODS: The expression of heme oxygenase-1 protein and messenger RNA was investigated at different time points following MCAO using immunohistochemistry, Western blotting, RT-PCR, and Northern blotting. RESULTS: Increased HO 1immunoreactivity was detected in hippocampal and cortical neurons after 1 hour of ischemia, and was also observed in astroglial cells. After 12 hours of ischemia, HO-1 was found in both neurons and glia in cerebral cortex and thalamus, and in striatal glia cells. Western blotting analysis show the expression of HO-1 protein in cortical neurons reached the peak after 12 hours of occlusion and decreased gradually, but was still detected at day 7 post-occlusion. The expression of messenger RNA was examined in the brains of rats subjected to permanent cerebral ischemia by semi-quantitative RT-PCR and Northern blotting. HO-1 mRNA transcription could be detected 1 hour after occlusion. After 1 to 6 hours of occlusion, the expression of HO-1 rose rapidly, reaching a peak at 12 hours post-occlusion, decreased gradually, and lasted until day 7 of occlusion. Although HO activity of cerebral tissue can be detected in both sham-operated group and operated groups, the HO activity in operated groups is much stronger than that in sham-operated group. CONCLUSIONS: The induction of HO-1 protein may protect cerebral tissues from ischemic damage.
BACKGROUND:Carbon monoxide has been regarded as a gaseous molecular messenger like nitric oxide. PURPOSE: To clarify the role of heme oxygenase-1 in the permanent cerebral ischemia at the protein and mRNA level. METHODS: The expression of heme oxygenase-1 protein and messenger RNA was investigated at different time points following MCAO using immunohistochemistry, Western blotting, RT-PCR, and Northern blotting. RESULTS: Increased HO 1immunoreactivity was detected in hippocampal and cortical neurons after 1 hour of ischemia, and was also observed in astroglial cells. After 12 hours of ischemia, HO-1 was found in both neurons and glia in cerebral cortex and thalamus, and in striatal glia cells. Western blotting analysis show the expression of HO-1 protein in cortical neurons reached the peak after 12 hours of occlusion and decreased gradually, but was still detected at day 7 post-occlusion. The expression of messenger RNA was examined in the brains of rats subjected to permanent cerebral ischemia by semi-quantitative RT-PCR and Northern blotting. HO-1 mRNA transcription could be detected 1 hour after occlusion. After 1 to 6 hours of occlusion, the expression of HO-1 rose rapidly, reaching a peak at 12 hours post-occlusion, decreased gradually, and lasted until day 7 of occlusion. Although HO activity of cerebral tissue can be detected in both sham-operated group and operated groups, the HO activity in operated groups is much stronger than that in sham-operated group. CONCLUSIONS: The induction of HO-1 protein may protect cerebral tissues from ischemic damage.
Authors: Cheol Hong Park; Tae Kyeong Shin; Ho Youn Lee; So Jung Kim; Won Suk Lee Journal: Korean J Physiol Pharmacol Date: 2011-04-30 Impact factor: 2.016
Authors: Simon Nagel; Michalis Papadakis; Ruoli Chen; Lisa C Hoyte; Keith J Brooks; Daniel Gallichan; Nicola R Sibson; Chris Pugh; Alastair M Buchan Journal: J Cereb Blood Flow Metab Date: 2010-04-21 Impact factor: 6.200
Authors: Tae Kyeong Shin; Mi Sun Kang; Ho Youn Lee; Moo Sang Seo; Si Geun Kim; Chi Dae Kim; Won Suk Lee Journal: Korean J Physiol Pharmacol Date: 2009-06-30 Impact factor: 2.016