In the present study, we hypothesized that 5-hydroxymethyl-2-furfural could attenuate ischemic brain damage by reducing oxidative injury. Thus, mice were subjected to bilateral common carotid artery occlusion to estab...In the present study, we hypothesized that 5-hydroxymethyl-2-furfural could attenuate ischemic brain damage by reducing oxidative injury. Thus, mice were subjected to bilateral common carotid artery occlusion to establish a model of permanent forebrain ischemia. The mice were intraperitoneally injected with 5-hydroxymethyl-2-furfura130 minutes before ischemia or 5 minutes after ischemia. The survival time of mice injected with 5-hydroxymethyl-2-furfural was longer compared with untreated mice. The mice subjected to ischemia for 30 minutes and reperfusion for 5 minutes were intraperitoneally injected with 5-hydroxymethyl-2-furfural 5 minutes prior to reperfusion, which increased superoxide dismutase content and reduced malondialdehyde content, similar to the effects of Edaravone, a hydroxyl radical scavenger used for the treatment of stroke. These findings indicate that intraperitoneal injection of 5-hydroxymethyl-2-furfural can prolong the survival of mice with permanent forebrain ischemia. This outcome may be mediated by its antioxidative effects.展开更多
Recent evidence exists that glucose transporter 3（GLUT3） plays an important role in the energy metabolism in the brain.Most previous studies have been conducted using focal or hypoxic ischemia models and have focuse...Recent evidence exists that glucose transporter 3（GLUT3） plays an important role in the energy metabolism in the brain.Most previous studies have been conducted using focal or hypoxic ischemia models and have focused on changes in GLUT3 expression based on protein and m RNA levels rather than tissue levels.In the present study,we observed change in GLUT3 immunoreactivity in the adult gerbil hippocampus at various time points after 5 minutes of transient forebrain ischemia.In the sham-operated group,GLUT3 immunoreactivity in the hippocampal CA1 region was weak,in the pyramidal cells of the CA1 region increased in a time-dependent fashion 24 hours after ischemia,and in the hippocampal CA1 region decreased significantly between 2 and 5 days after ischemia,with high level of GLUT3 immunoreactivity observed in the CA1 region 10 days after ischemia.In a double immunofluorescence study using GLUT3 and glial-fibrillary acidic protein（GFAP）,we observed strong GLUT3 immunoreactivity in the astrocytes.GLUT3 immunoreactivity increased after ischemia and peaked 7 days in the dentate gyrus after ischemia/reperfusion.In a double immunofluorescence study using GLUT3 and doublecortin（DCX）,we observed low level of GLUT3 immunoreactivity in the differentiated neuroblasts of the subgranular zone of the dentate gyrus after ischemia.GLUT3 immunoreactivity in the sham-operated group was mainly detected in the subgranular zone of the dentate gyrus.These results suggest that the increase in GLUT3 immunoreactivity may be a compensatory mechanism to modulate glucose level in the hippocampal CA1 region and to promote adult neurogenesis in the dentate gyrus.展开更多
Artemisia capillaris Thunberg is a medicinal plant used as a traditional medicine in many cultures. It is an effective remedy for liver problems including hepatitis. Recent pharmacological reports have indicated that ...Artemisia capillaris Thunberg is a medicinal plant used as a traditional medicine in many cultures. It is an effective remedy for liver problems including hepatitis. Recent pharmacological reports have indicated that Artemisia species can exert various neurological effects. Previously, we reported a memory-enhancing effect of Artemisia species. However, the mechanisms underlying the neuroprotective effect of A. capillaris(AC) are still unknown. In the present study, we investigated the effect of an ethanol extract of AC on ischemic brain injury in a mouse model of transient forebrain ischemia. The mice were treated with AC for seven days, beginning one day before induction of transient forebrain ischemia. Behavioral deficits were investigated using the Y-maze. Nissl and Fluoro-jade B staining were used to indicate the site of injury. To determine the underlying mechanisms for the drug, we measured acetylcholinesterase activity. AC(200 mg·kg-1) treatment reduced transient forebrain ischemia-induced neuronal cell death in the hippocampal CA1 region. The AC-treated group also showed significant amelioration in the spontaneous alternation of the Y-maze test performance, compared to that in the untreated transient forebrain ischemia group. Moreover, AC treatment showed a concentration-dependent inhibitory effect on acetylcholinesterase activity in vitro. Finally, the effect of AC on forebrain ischemia was blocked by mecamylamine, a nonselective nicotinic acetylcholine receptor antagonist. Our results suggested that in a model of forebrain ischemia, AC protected against neuronal death through the activation of nicotinic acetylcholine receptors.展开更多
基金supported by the National Basic Research Program of China (973 Program),No.2003CB517104the National Natural Science Foundation of China,No.30973513+3 种基金Beijing Municipal Science and Technology Program,No.D0206001043191the Natural Science Foundation of Beijing,No.7112061Beijing Key Foundation of Traditional Chinese Medicine,No.KJTS2011-04Beijing Health and Technical Personal of High-Level Plan,No.2009-3-66
文摘In the present study, we hypothesized that 5-hydroxymethyl-2-furfural could attenuate ischemic brain damage by reducing oxidative injury. Thus, mice were subjected to bilateral common carotid artery occlusion to establish a model of permanent forebrain ischemia. The mice were intraperitoneally injected with 5-hydroxymethyl-2-furfura130 minutes before ischemia or 5 minutes after ischemia. The survival time of mice injected with 5-hydroxymethyl-2-furfural was longer compared with untreated mice. The mice subjected to ischemia for 30 minutes and reperfusion for 5 minutes were intraperitoneally injected with 5-hydroxymethyl-2-furfural 5 minutes prior to reperfusion, which increased superoxide dismutase content and reduced malondialdehyde content, similar to the effects of Edaravone, a hydroxyl radical scavenger used for the treatment of stroke. These findings indicate that intraperitoneal injection of 5-hydroxymethyl-2-furfural can prolong the survival of mice with permanent forebrain ischemia. This outcome may be mediated by its antioxidative effects.
基金supported by Basic Science Research Program through the National Research Foundation of Korea(NRF) funded by the Ministry of Education,No.NRF-2013R1A1A2059364,NRF-2015R1D1A3A01020635)by 2013 Research Grant from Kangwon National Universitypartially supported by the Research Institute for Veterinary Science,Seoul National University
文摘Recent evidence exists that glucose transporter 3（GLUT3） plays an important role in the energy metabolism in the brain.Most previous studies have been conducted using focal or hypoxic ischemia models and have focused on changes in GLUT3 expression based on protein and m RNA levels rather than tissue levels.In the present study,we observed change in GLUT3 immunoreactivity in the adult gerbil hippocampus at various time points after 5 minutes of transient forebrain ischemia.In the sham-operated group,GLUT3 immunoreactivity in the hippocampal CA1 region was weak,in the pyramidal cells of the CA1 region increased in a time-dependent fashion 24 hours after ischemia,and in the hippocampal CA1 region decreased significantly between 2 and 5 days after ischemia,with high level of GLUT3 immunoreactivity observed in the CA1 region 10 days after ischemia.In a double immunofluorescence study using GLUT3 and glial-fibrillary acidic protein（GFAP）,we observed strong GLUT3 immunoreactivity in the astrocytes.GLUT3 immunoreactivity increased after ischemia and peaked 7 days in the dentate gyrus after ischemia/reperfusion.In a double immunofluorescence study using GLUT3 and doublecortin（DCX）,we observed low level of GLUT3 immunoreactivity in the differentiated neuroblasts of the subgranular zone of the dentate gyrus after ischemia.GLUT3 immunoreactivity in the sham-operated group was mainly detected in the subgranular zone of the dentate gyrus.These results suggest that the increase in GLUT3 immunoreactivity may be a compensatory mechanism to modulate glucose level in the hippocampal CA1 region and to promote adult neurogenesis in the dentate gyrus.
基金supported by Dong-A University Research Supporting Program
文摘Artemisia capillaris Thunberg is a medicinal plant used as a traditional medicine in many cultures. It is an effective remedy for liver problems including hepatitis. Recent pharmacological reports have indicated that Artemisia species can exert various neurological effects. Previously, we reported a memory-enhancing effect of Artemisia species. However, the mechanisms underlying the neuroprotective effect of A. capillaris(AC) are still unknown. In the present study, we investigated the effect of an ethanol extract of AC on ischemic brain injury in a mouse model of transient forebrain ischemia. The mice were treated with AC for seven days, beginning one day before induction of transient forebrain ischemia. Behavioral deficits were investigated using the Y-maze. Nissl and Fluoro-jade B staining were used to indicate the site of injury. To determine the underlying mechanisms for the drug, we measured acetylcholinesterase activity. AC(200 mg·kg-1) treatment reduced transient forebrain ischemia-induced neuronal cell death in the hippocampal CA1 region. The AC-treated group also showed significant amelioration in the spontaneous alternation of the Y-maze test performance, compared to that in the untreated transient forebrain ischemia group. Moreover, AC treatment showed a concentration-dependent inhibitory effect on acetylcholinesterase activity in vitro. Finally, the effect of AC on forebrain ischemia was blocked by mecamylamine, a nonselective nicotinic acetylcholine receptor antagonist. Our results suggested that in a model of forebrain ischemia, AC protected against neuronal death through the activation of nicotinic acetylcholine receptors.
