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1.
Journal of Southern Medical University ; (12): 1268-1271, 2010.
Article in Chinese | WPRIM | ID: wpr-336203

ABSTRACT

<p><b>OBJECTIVE</b>To observe the temporal and spatial changes in the distribution of Ca2+ in the rat brain following focal cerebral ischemia injury and explore the protective effect of puerarin against calcium overload.</p><p><b>METHODS</b>Focal cerebral ischemia was induced by middle cerebral artery occlusion in rats. After cerebral ischemia, puerarin was administered in the rats at different time points. The volume of ischemic cerebral tissue was assessed by TTC staining, and the fluorescence intensity of Ca2+ in the cortex and corpora striata was determined under laser scanning confocal microscope.</p><p><b>RESULTS</b>The fluorescence intensity of Ca2+ in the infracted cortex and corpora striata begun to increase 2 h after the ischemia and was further enhanced with the prolongation of the ischemic time. No significance was found in the fluorescence intensity of Ca2+ between the cortex and corpora striata. The fluorescence intensity of Ca2+ in the infarcted corpora striata was obviously higher than that in the cortex after ischemia. Compared with that in the ischemic model group, the fluorescence intensity of Ca2+ in the infarcted cortex and corpora striata decreased significantly at 2 and 12 h following puerarin intervention (P<0.05).</p><p><b>CONCLUSION</b>Puerarin treatment can relieve calcium overload, reduce cerebral ischemic volume and play a neuroprotective role against focal cerebral ischemia. Twelve hours following cerebral ischemic injury may be the time window for administering puerarin intervention.</p>


Subject(s)
Animals , Male , Rats , Brain , Metabolism , Brain Ischemia , Drug Therapy , Metabolism , Calcium , Metabolism , Calcium-Transporting ATPases , Metabolism , Infarction, Middle Cerebral Artery , Drug Therapy , Metabolism , Isoflavones , Pharmacology , Therapeutic Uses , Neuroprotective Agents , Pharmacology , Therapeutic Uses , Random Allocation , Rats, Sprague-Dawley
2.
Chinese journal of integrative medicine ; (12): 54-59, 2009.
Article in English | WPRIM | ID: wpr-236232

ABSTRACT

<p><b>OBJECTIVE</b>To observe the effect of puerarin on the learning-memory disorder after global cerebral ischemia-reperfusion injury in rats, and to explore its mechanism of action.</p><p><b>METHODS</b>The global cerebral ischemia-reperfusion injury model was established using the modifified Pulsinelli four-vessel occlusion in Sprague-Dawley rats. Rats were intraperitoneally injected with puerarin (100 mg/kg) 1 h before ischemia and once every 6 h afterwards. The learning-memory ability was evaluated by the passive avoidance test. The dynamic changes of the cell counts of apoptosis and positive expression of Bcl-2 in the hippocampus CA1 region were determined by the TUNEL and immunohistochemical methods, respectively.</p><p><b>RESULTS</b>(1) Compared with the reperfusion group, the step through latency (STL) in the passive avoidance test in the puerarin group was prolonged signifificantly (P<0.01). (2) The apoptotic neurons were injured most severely on the 3rd day in the hippocampal CA1 region after global ischemia and reperfusion. In the puerarin group, the number of apoptotic cells decreased at respective time points after ischemia-reperfusion (P<0.01). (3) The level of positive expression of Bcl-2 varied according to the duration of reperfusion and the peak level occurred on day 1 in the hippocampal CA1 region after global cerebral ischemia. Compared with the reperfusion group, the expression of Bcl-2 in the puerarin group was up-regulated at the respective time points after ischemia reperfusion (P<0.01), reaching the peak on day 1.</p><p><b>CONCLUSIONS</b>Puerarin could improve the learning-memory ability after global cerebral ischemia and reperfusion in rats. The protective mechanism might be related to the effect of inhibiting or delaying the cell apoptosis through up-regulating the expression of Bcl-2 after ischemia and reperfusion.</p>


Subject(s)
Animals , Rats , Apoptosis , Brain Ischemia , Drug Therapy , Hippocampus , Pathology , Isoflavones , Pharmacology , Therapeutic Uses , Learning , Memory Disorders , Drug Therapy , Models, Biological , Protective Agents , Pharmacology , Therapeutic Uses , Proto-Oncogene Proteins c-bcl-2 , Metabolism , Reaction Time , Reperfusion Injury , Drug Therapy
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