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<p><b>OBJECTIVE</b>To investigate the effect of dauricine on the apoptosis of neuronal cells and the expression of apoptosis-related proteins in the brain penumbra of rats induced by transient focal cerebral ischemia-reperfusion injury.</p><p><b>METHOD</b>Male SD rats were randomly divided into five groups: sham group (Sham), model group (Model), and Dauricine groups of low, middle and high doses. To make the transient focal cerebral ischemia-reperfusion injury model, the middle cerebral artery on the right side of rat was occluded by inserting a nylon suture through the internal carotid artery for 1 h, followed by reperfusion for 24 h after withdrawing the suture. Dauricine groups, different doses of Dauricine (2.5, 5, 10 mg x kg(-1) as low, middle and high dose respectively) were administered intraperitoneally at the beginning of the cerebral ischemia, and at 11 h and 23 h after reperfusion. At the same time, Sham group and Model group was administered saline as controls. Brain samples of rats were treated with paraformaldehyde perfusion fixation 24 h after blood reperfusion and then collected for making pathological sections. Apoptotic changes of neuronal cells in the brain penumbra of rat were evaluated in situ by terminal deoxyribonucleotidyl transferasemediated dUTP-digoxigenin nick end-labelling (TUNEL). Cytochrome C (Cyt-C) release and the expression of caspase -3 and caspase -9 proteins of the ischemic-reperfusion brain tissue were determined by immunohistochemistry assay.</p><p><b>RESULT</b>TUNEL-positive cells in groups of middle and high doses of dauricine (18.9 +/- 2.02 and 15.9 +/- 2.9 cells/mm2 respectively) decreased significantly compared with model group (25.5 +/- 3.3 cells/mm2, P<0.05). Cyt-C release and the expression of caspase-3 and caspase-9 proteins in groups of middle and high doses of dauricine were also inhibited compared with Model group (P<0.01).</p><p><b>CONCLUSION</b>The mechanism of the neuroprotective effect of dauricine after cerebral ischemia-reperfusion injury may parly, related with an inhibition of neuronal cells apoptosis in the penumbra.</p>
Subject(s)
Animals , Male , Rats , Apoptosis , Benzylisoquinolines , Pharmacology , Caspases , Metabolism , Cytochromes c , Metabolism , Dose-Response Relationship, Drug , Gene Expression Regulation , Ischemic Attack, Transient , General Surgery , Neuroprotective Agents , Pharmacology , Reperfusion Injury , Metabolism , Pathology , Tetrahydroisoquinolines , PharmacologyABSTRACT
Aim To investigate glutamate-induced [ Ca2 + ] i changes in cultured rat neonatal cortical astrocytes after hypoxia/reoxygenation, H2O2 or high concentration of L-glutamate injury. In the meantime, the effects of Gingko biloba extract (GbE) were examined. Methods [ Ca2+ ]i changes in astrocytes were monitored by laser scanning confocal microscopy with the Ca2+ sensitive fluorescent probe [ Ca2 + ] i, but decrease by ( 3.3 ± 1.6) %, (81 ± 11 ) % and ( 81 ± 7 ) %, respectively. Pretreatment with H2O2 or high concentration of L-glutamate injury were ( 135 ± 98 ) %, ( 117 ± 93 ) % and ( 89 ± 36) %,different injury. Conclusion Hypoxia/reoxygenation, H2O2 and high concentration of L-glutamate impaired astrocytes' response to exogenous L-glutamate, and then bidirectional communication between astrocytes and neurons could not take place. GbE could improve the abnormal responses and maintain the normal function of astroglical network. These effects support that GbE has potential beneficial actions against brain injury.
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Aim To investigate the protective effects of dihydrolycorine on hypoxia/reoxygenation (H/R) injury in cultured neonatal rat cardiomyocytes. Methods The hypoxia/ reoxygenation injury model of cultured neonatal rat cardiomyocytes was developed. The cell livability, the activity of lactate dehdrogenase (LDH) and superoxide dismutase (SOD), and the content of malondialdehyde (MDA) were determined in the cultured neonatal rat cardiomyocytes injured by H/R. Results Compared with normal group, the cell livability and the SOD activity of model group were decreased respectively, whereas the activity of LDH and the content of MDA of model group were increased significantly (P
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The use-dependent characteristics of daurisoline on monophasic action potentials (MAP) of the left ventricle of the rabbit heart in situ were recorded with MAP recording technique. The results showed that daurisoline decreased monophasic action potential amplitude (MAPA) and prolonged monophasic action potential duration at the 50% and 90% (MAPD50, MAPD90), effective refractory period (ERP), ERP/MAPD90 at the steady-state cycle lengths of 240, 210, 180 ms. The percent of prolongation of MAPD50 was 12.8±2.9, 9.5±2.6, 9.0±1.6, that of MAPD90 was 10.9±2.6, 7.5±2.4, 6.5±2.7, that of ERP was 25.7±4.3, 18.5±4.1, 24.2±7.2, and that of ERP/MAPD90 was 13.7±4.5, 10.2±2.2, 16.1±5.1, respectively. Its effect showed no relation to frequency (n=6, P>0.05). The effects of sotalol on MAP were similar to that of daurisoline, but it prolonged MAPD90 and ERP in a reverse use-dependent manner (P<0.05). It is concluded that daurisoline has no use-dependent effects on MAP of rabbit hearts.
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0.05 ). After once injection both observers considered the number of clearly recognized endocardial border segments increased significantly. The number evaluated by observers A increased from 2.68 ? 0.95 to 5.99 ? 0.10 while from 2.82 ? 1.03 to 5.99 ? 0.11 by observers B( P 0.05 ). The average contrast enhancement rate of LV endocardial border was 99.7 %. Perfluoropropane-albumin microsphere injection had no significant effection on vital signs such as blood prssure, heart rate and respiration. Electrocardiogram didn′t change markedly and the variance of the laboratory findings like blood and urine routine examination, hepatic and renal function was in normal range. Only one case( 0.33 %) had slight side-effects who suffered from mild nausea and diarrhea, which suggested the clinical safety of this contrast agent. Conclusions Perfluoropropane-albumin microsphere injection could enhance the resolution of LV endocardial borders and make the judgement of regional myocardial movement easier. It has little side-effects and will be appropriate for clinical use.
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AIM To investigate the protective effects of dauricine on anoxia and acute cerebral ischemia-reperfusion in mice. METHODS In this study, anoxia was induced by close normobaric hypoxia to search the effects of dauricine on the survival time of mice. The activities of SOD, GSH-Px and levels of MDA in cortex or mitochondria, the activities of cortex LDH and mitochondria ATPase were all measured by ELISA-Reader and spectrophotography. RESULTS ① Dauricine prolonged the survival time of mice in the close normobaric hypoxia, among all doses, Dauricine 60 mg?kg -1 and 120 mg?kg -1 had significant most effects (P