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PAR-1拮抗剂SCH79797对SAH大鼠早期脑损伤的保护作用及对BDNF、NGF表达的影响 被引量:7
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作者 李育鑫 袁绍纪 +4 位作者 朱伟杰 于峰 李博 王奎重 卢培刚 《中华神经医学杂志》 CAS CSCD 北大核心 2016年第7期700-704,共5页
目的探讨凝血酶受体-1(PAR-1)拮抗剂SCH79797对蛛网膜下腔出血(SAH)大鼠早期脑损伤的保护作用及可能机制。方法雄性SPF级SD大鼠54只按随机数字表法分为假手术组、SAH组、治疗组,每组18只。后2组采用枕大池单次注血法建立大鼠SAH模... 目的探讨凝血酶受体-1(PAR-1)拮抗剂SCH79797对蛛网膜下腔出血(SAH)大鼠早期脑损伤的保护作用及可能机制。方法雄性SPF级SD大鼠54只按随机数字表法分为假手术组、SAH组、治疗组,每组18只。后2组采用枕大池单次注血法建立大鼠SAH模型,治疗组在造模成功后给予SCH79797(25μg/kg)腹腔注射。各组大鼠于术后24h进行神经功能缺损评分,然后断头取脑,采用干湿重法检测脑组织含水量,采用ELISA法检测海马区脑组织脑源性神经营养因子(BDNF)、神经生长因子(NGF)含量,采用免疫荧光染色检测BDNF、NGF表达。结果与SAH组比较,治疗组神经功能缺损评分明显增高(12.11±2.62vs14.59±2.24),脑组织含水量明显减少(83.01%±0.38%vs79.79%±0.44%),海马区脑组织BDNF、NGF含量明显增加[(100.15±59.13)pg/mLvs(368.00±137.52)pg/mL;(33.44~2.21)pg/mLvs(37.49±2.29)pg/mL],BDNF、NGF免疫荧光染色强度明显增高(41.65±1.50vs91.40±1.30;23.50±1.70vs30.65±1.80),差异均有统计学意义(P〈0.05)。结论PAR.1拮抗剂SCH79797对SAH大鼠早期脑损伤有脑保护作用,其作用机制可能涉及有效上调BDNF、NGF表达水平。 展开更多
关键词 蛛网膜下腔出血 早期脑损伤 凝血酶受体-1 拮抗剂sch79797 脑源性 神经营养因子 神经生长因子
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A protease-activated receptor 1 antagonist protects against global cerebral ischemia/reperfusion injury after asphyxial cardiac arrest in rabbits 被引量:2
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作者 Jing-ning Yang Jun Chen Min Xiao 《Neural Regeneration Research》 SCIE CAS CSCD 2017年第2期242-249,共8页
Cerebral ischemia/reperfusion injury is partially mediated by thrombin, which causes brain damage through protease-activated receptor 1(PAR1). However, the role and mechanisms underlying the effects of PAR1 activati... Cerebral ischemia/reperfusion injury is partially mediated by thrombin, which causes brain damage through protease-activated receptor 1(PAR1). However, the role and mechanisms underlying the effects of PAR1 activation require further elucidation. Therefore, the present study investigated the effects of the PAR1 antagonist SCH79797 in a rabbit model of global cerebral ischemia induced by cardiac arrest. SCH79797 was intravenously administered 10 minutes after the model was established. Forty-eight hours later, compared with those administered saline, rabbits receiving SCH79797 showed markedly decreased neuronal damage as assessed by serum neuron specific enolase levels and less neurological dysfunction as determined using cerebral performance category scores. Additionally, in the hippocampus, cell apoptosis, polymorphonuclear cell infiltration, and c-Jun levels were decreased, whereas extracellular signal-regulated kinase phosphorylation levels were increased. All of these changes were inhibited by the intravenous administration of the phosphoinositide 3-kinase/Akt pathway inhibitor LY29004(3 mg/kg) 10 minutes before the SCH79797 intervention. These findings suggest that SCH79797 mitigates brain injury via anti-inflammatory and anti-apoptotic effects, possibly by modulating the extracellular signal-regulated kinase, c-Jun N-terminal kinase/c-Jun and phosphoinositide 3-kinase/Akt pathways. 展开更多
关键词 nerve regeneration protease-activated receptor 1 global cerebral ischemia/reperfusion cardiac arrest neuroprotection sch79797 apoptosis inflammation neuron specific enolase hippocampus neural regeneration
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