Neuroprotective effects of LBP on brain ischemic reperfusion neurodegeneration

来源 :中国药理学与毒理学杂志 | 被引量 : 0次 | 上传用户:wuddy
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OBJECTIVE The present study was conducted to investigate whether LBP had a protective effect on cerebral ischemic reperfusion injury and to determine the possible mechanisms.METHODS Male Kunming(KM) mice were used to make the model cerebral artery occlusion/reperfusion(MCAO/R).The behavioral test was used to measure neurological deficit scores for evaluation of ischemic reperfusion damage of brain.The change of electroencephalograph(EEG) was monitored by Model SMUP-E Bio-electric Signals Processing System.The infarction area of brain was assessed in brain slices with 2% solution of 2,3,5-triphenyl tetrazolium chloride(TTC).Spectrophotometric assay was used to determine the activities of superoxide dismutase(SOD),glutathione peroxidase(GSH-Px),catalase(CAT) and lactate dehydrogenase(LDH),contents of malondialdehyde(MDA) and adenosine triphosphate(ATP) of the brain.RESULTS Results showed that LBP at doses of 20 and 40 mg·kg-1 markedly decreased the neurological deficit scores and the infarction area in MCAO/R mice.At the same time,LBP significantly decreased MDA content,and increased SOD,GSH-Px,CAT,LDH activities in ischemic reperfusion brain.CONCLUSION These suggest that LBP might act as a potential neuroprotective agent against the cerebral reperfusion-induced injury in the brain through reducing lipid peroxides,scavenging free radicals,and improving the energy metabolism. OBJECTIVE The present study was conducted to investigate whether LBP had a protective effect on cerebral ischemic reperfusion injury and to determine the possible mechanisms. METHODS Male Kunming (KM) mice were used to make the model cerebral artery occlusion / reperfusion (MCAO / R). The behavioral test was used to measure neurological deficit scores for evaluation of ischemic reperfusion damage of brain. The change of electroencephalograph (EEG) was monitored by Model SMUP-E Bio-electric Signals Processing System. The infarction area of ​​the brain was assessed in brain slices with 2% solution of 2,3,5-triphenyl tetrazolium chloride (TTC). Spectrophotometric assay was used to determine the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT) and lactate dehydrogenase ) contents of malondialdehyde (MDA) and adenosine triphosphate (ATP) of the brain .RESULTS Results showed different LBP at doses of 20 and 40 mg · kg-1 markedly decreased the neurological deficit scores and the in farction area in MCAO / R mice. At the same time, LBP decreased MDA content, and increased SOD, GSH-Px, CAT, LDH activities in ischemic reperfusion brain. CONCLUSION These suggest that LBP might act as a potential neuroprotective agent against the cerebral reperfusion-induced injury in the brain through reducing lipid peroxides, scavenging free radicals, and improving the energy metabolism.
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