ABSTRACT
<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 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
ABSTRACT
AIM: To probe the effect of azelastine hydrochloride on experimental asthma and its mechanism. METHODS: Experimental asthma models of guinea pigs induced by histamine and acetylcholine in vivo as well as guinea pig tracheal spirals in vitro were used in this experiment. RESULTS: Azelastine hydrochloride inhibited asthma induced by histamine and acetylcholine in guinea pigs in a dose dependent manner, prolonged the incubation period of histamine and acetylcholine induced asthma (P