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中药复方护脑素在大鼠急性脑缺血模型中的作用机制 被引量:5
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作者 钟平 杨任民 《中国临床康复》 CSCD 2003年第19期2656-2657,共2页
目的研究以麻黄、山栀子、黄连、厚朴、白术、桂枝、三七为主要成分的中药复方护脑素改善脑部微循环及脑保护的作用机制。方法将Wistar大鼠随机分成3组,模型组(结扎两侧颈总动脉)、护脑素组(颈总动脉结扎前半小时腹腔灌注护脑素混悬液)... 目的研究以麻黄、山栀子、黄连、厚朴、白术、桂枝、三七为主要成分的中药复方护脑素改善脑部微循环及脑保护的作用机制。方法将Wistar大鼠随机分成3组,模型组(结扎两侧颈总动脉)、护脑素组(颈总动脉结扎前半小时腹腔灌注护脑素混悬液)和假手术组,每组10只。用组织血流量仪测定各组手术前后局部脑血流量(r-CBF),用硝酸还原法测定血浆一氧化氮(NO),用放射免疫分析法检测血浆内皮素1(ET-1)。手术后2h将大鼠处死,取出脑组织,测定脑匀浆中NO与ET-1含量。结果①rCBF值:模型组为(202±38)mL/(min·kg),显著低于假手术组(635±81)mL/(min·kg)(t=15.34,P<0.001)和护脑素组(267±47)mL/(min·kg)(t=3.33,P<0.05)。②护脑素组血浆NO(2.6±0.5)mol/L高于模型组(2.1±0.8)mol/L(t=4.23,P<0.05)。模型组血浆ET-1(540.0±101.0)ng/L高于假手术组(349.0±26.0)ng/L,(t=6.14,P<0.05)和护脑素组(427.0±83.0)ng/L,(t=2.73,P<0.05)。③模型组组织匀浆中NO(406.0±163.5)mol/L和ET-1(11.4±2.0)ng/L分别高于假手术组的(177.4±63.3)mol/L,(8.1±1.5)ng/L,(t=4.13,4.04,P<0.005)和护脑素组的(207.2±113.4)mol/L,(8.3±1.7)ng/L(t=3.16,3.64,P<0.005)。结论护脑素在急性脑缺血模型中可通过NO、ET-1的参与,改善脑部微循环。 展开更多
关键词 中药复方 护脑素 大鼠 急性缺血 动物模型 部微循环
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护脑素胶囊抗脑缺血作用的实验研究
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作者 范玉新 杨任民 +3 位作者 韩咏竹 晏义平 许冠荪 王钦茂 《中国中西医结合杂志》 CAS CSCD 北大核心 1996年第S1期54-56,279,共4页
本研究应用大鼠脑缺血及脑缺血后再灌注模型,探讨了护脑素胶囊的药效学机制。结果:本品能显著阻止脑缺血后脑组织兴奋性氨基酸(EAA)释放,提高脑缺血后再灌注模型动物红细胞内超氧化物歧化酶(SOD)活性,降低血清过氧化脂质(LPO)含量,同时... 本研究应用大鼠脑缺血及脑缺血后再灌注模型,探讨了护脑素胶囊的药效学机制。结果:本品能显著阻止脑缺血后脑组织兴奋性氨基酸(EAA)释放,提高脑缺血后再灌注模型动物红细胞内超氧化物歧化酶(SOD)活性,降低血清过氧化脂质(LPO)含量,同时还能增加脑缺血后再灌注损伤低灌注期局部脑血流量(rCBF),抗迟发性低灌注,从而减轻迟发性神经元坏死(DND),其作用与溶媒组比较均有显著或极显著差异(P<0.05~0.01)。提示:护脑素胶囊可多环节打断脑缺血后之病理生理过程,对脑缺血损伤有明显保护作用。 展开更多
关键词 护脑素胶囊 缺血 兴奋性氨基酸 超氧化物歧化酶 过氧化脂质 局部血流量
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Neuroprotective effect of sodium ferulate on transient focal cerebral ischemia by weakening activation of postsynaptic density-95 in rats 被引量:2
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作者 王强 陈绍洋 +2 位作者 熊利泽 金卫林 杨静 《Chinese Journal of Traumatology》 CAS 2005年第5期297-302,共6页
Objective: To investigate the effects of sodium ferulate (SF), an intravenous drug made from traditional Chinese herbs, on activation of postsynaptic density-95 (PSD-95) and neuroprotection after transient cerebr... Objective: To investigate the effects of sodium ferulate (SF), an intravenous drug made from traditional Chinese herbs, on activation of postsynaptic density-95 (PSD-95) and neuroprotection after transient cerebral artery occlusion in rats. Methods: Forty-six male Sprague-Dawley rats were randomized into 2 groups ( n = 23 in each group) : the control group and the SF group. After anesthesia, the middle cerebral artery occlusion (MCAO) was conducted with the intraluminal filament technique. The neurological deficit was assessed with the method devised by Bederson et al.^ 8 The 2, 3, 4-triphenyltetrazolium chloride staining was used to assess the infarct volume. We adopted a modified six-point scale to conduct neurobehavioral evaluation. Immediately the activation of postsynaptic density-95 ( PSD- 95 ) was studied with Western blot analysis system in the cortex and striatum of rat brain. Results : The neurologic deficit score of the SF group decreased substantially compared with that of the control group ( P 〈0.05). The infarct volume of the control group (168.1 mm^3 ± 42.2 mm^3) was significantly larger than that of the SF group (61.5 mm^3 ± 28.7 mm^3 ) at 24 hours after reperfusion (P 〈 0.01 ). And the rats showed some neurological deficit. The activity of PSD-95 in the SF group at most timepoints was less than that in the control group. No upregulation of PSD-95 protein could be detected in the contralateral cortex. Conclusions : Sodium ferulate can induce a neuroproteetive effect against the transient focal cerebral isehemie injury and weaken the activation of PSD-95 in isehemie area after MCAO. 展开更多
关键词 Brain ischemia RATS Sodium ferulate Postsynaptic density-95 PSD-95
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