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Aim To study the effect of gamma-hydroxybutyric acid receptor(GHBR ) on neuronal apoptosis suffering from focal cerebral ischemia-reperfusion injury in rats. Methods The male Sprague-Dawley rats weighing 240～280 g were randomly divided into seven groups: sham operation group(sham), ischemia-reperfusion group(Isc/R) ,NCS-356 160、320、640 ?g?kg-1 group(N1、N2、N3),NCS-382 640+NCS-356 640 ?g?kg-1 group(NCS-382+N3),and nimodipine 600 ?g?kg-1 group(Nim).The middle cerebral artery occlusion(MCAO) model invented by Zea Longa with modifications was adopted. The experiment was divided into two parts after ischemia reperfusion for 24h:In the first part,we measured the cerebral expression of Bax, Bcl-2, Caspase-3 by immuneohistochemical method. In the second part,we measured neuronal apoptotic rate by flow cytometry in the ischemic cortex region. Results The expression rate of Bcl-2 and Bcl-2/Bax ratio of N1,N2,N3 and Nim groups were all higher than that of Isc/R group(P
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AIM To investigate the effects of melatonin (MT) on glutathione peroxidase(GPx), superoxide dismutase(SOD) activities and malondialdehyde(MDA) contents in the cerebrum of cerebral ischemia-reperfusion gerbils, so as to explore the protective mechanisms of MT. METHODS Cerebral ischemia-reperfusion model was made by 10 min occlusion of bilateral carotid arteries of gerbil. MT was administered intraperitoneally 30 min prior to the onset of ischemia. After 1 h reperfusion, bilateral cortex and striatum were taken out for measurement of GPx, SOD and MDA. RESULTS Ischemia-reperfusion lowered the activities of GPx and SOD in cerebral cortex and striatum. Conversely, it elevated the contents of MDA in both areas. Treatment with MT at 5, 10, or 20 mg?kg -1 partly reversed these effects. CONCLUSION MT provides protective effect against cerebral ischemia-reperfusion injury by protecting GPx and SOD activities and reducing the lipid peroxidation.
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AIM: To investigate the relationship between the protective effect of sodium oxybate on neuronal damage induced by hypoxia reoxygenation and GABA A receptor in primary cultured rat cortical neurons. METHODS: The primary cultured rat cortical neurons were used to make the hypoxia reoxygenation damage model. The morphology of cell was observed. The lactate dehydrogenase (LDH) effluxed into the media as an indicator of neuronal injury was detected after 6 h of the reoxygenation injuries. The malonyldialdehyde (MDA) contents, superoxide dismutase (SOD) and glutathione peroxidase (GPX) activities were determined at the same time. RESULTS: The hypoxia reoxygenation caused neuronal swelling and widespread neuronal degeneration, increased LDH efflux and MDA contents, and decreased SOD and GPX activities. Sodium oxybate assuaged neuron damage, decreased LDH efflux and MDA contents (P
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AIM:To study the protective effects of penehyclidine hydrochloride(PHC) on transient forebrain ischemia reperfusion injury in gerbils.METHODS:The model of transient forebrain ischemia reperfusion was established in gerbils by bilateral carotid artery clamping.The effects of PHC on neurological function scores and the morphous of hippocampal pyramidal neuron of gerbils were observed after receiving transient forebrain ischemia reperfusion.SOD activities and contents of MDA in the hippocampus and cortex of gerbils were measured.RESULTS:In the groups of PHC(0.08),(0.24)(mg?kg~(-1)) and atropine,the stroke index was decreased,compared with the ischemia-reperfusion group after the gerbils received transient forebrain ischemia reperfusion for six hours.PHC could reduce the degree of injury in hippocampal pyramidal neuron after ischemia reperfusion for three days.CONCLUSION: PHC has protective effects on transient forebrain ischemia reperfusion injury in gerbils.
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AIMTo study the protective effect of sodium oxybate (SO) against focal cerebral ischemia-reperfusion injury in rats, and the relationship between the effects of SO and ?-aminobutyric acid (GABA). METHODSThe reversible middle cerebral artery occlusion (MCAO)model in rats was established to investigate the role of SO. The scores of neurological deficits was detected by Longa EZ method in MCAO rats. The extracellular levels of glutamate (Glu) and GABA in CSF were measured by high performance liquid chromatography-fluorometer (HPLC-FR) method, and the weight of cerebral infraction was detected. RESULTSThe scores of neurological deficits and the weight of cerebral infraction markedly decreased by SO while the ratio of GABA/Glu obviously increased administered SO in MCAO rats. CONCLUSIONSSO could prevent MCAO rats from ischemia-reperfusion injury, the protective effect is related to SO keeping dynamic balance of excition-inhibition, and persisting inhibition-depended effect.
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AIM To investigate the protective effect of sodium gamma-hydroxybutyrate (?-OH) against cerebral ischemia-reperfusion injury in gerbils and the neuroprotective mechanism of ?-OH. METHODS The occlusion of bilateral carotid arteries of gerbil was used to make the cerebral ischemia-reperfusion models. Different doses of ?-OH were administered intraperitoneally 40 min prior to the onset of ischemia. After 10 min ischemia and 1 h reperfusion, bilateral hippocampus, cortex and striatum were taken out to measure ATPase, SOD and MDA. RESULTS The contents of MDA markedly elevated while Na +,K +-ATPase, Ca 2+ -ATPase and SOD activities decreased in hippocampus, cortex and striatum 1 h after ischemia-reperfusion. ?-OH administered prior to ischemia can partly reverse the elevation of MDA contents and the reduction of SOD activities. ?-OH given after ischemia can still provide partly protective effect. CONCLUSION ?-OH provides significant protective effect against cerebral ischemia-reperfusion injury by protecting ATPase and SOD activities, deleting free radicals and reducing the lipid peroxidation.
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Bepridil hydrochloride(Bep) hydrochloride is a new , long - acting antianginal and antiarrhythmic agent. Through the observation of ∑ST.NST.and NQ of ECG or nitro blue tetrazolium chloride staining, we studied the effect of Bep on liga-tion of the left coronary artery in rabbits and the myocardial ischemia induced by isopre-naline in rats. The results showed that in the groups treated with Hep andpropranolol theisoelectric level was facilitated. ∑ST.NST, NQ, thecreatine phosphokinase values and the weight percentage of infarcted myocardium were decreased. The myocardial ischemic injury was decreased by histopathological stud-
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Bepridil (10mg ? kg-1) iv elevated the threshold dose of ouabain (15ug ? min-1 iv) in guinea-pig and aconitine (10?g ? kg-1 ? min-1 iv) in rat induced ventricular extrasystole, ventricular tachycardia, ventricular fibrillation and cardiac arrest. It shortened the duration of arrhythmia elicitde by Adr (50ug ? Kg-1 iv) in conscious rabbits and by BaCl2 (3mg ? kg-1 iv) in rats. It is also effective in preventing reperfusion-induced arrhythmias in aneasthetized rats.