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作 者:谢瑱 张琛[1] 赵海波[1] 史明[1] 赵钢[1]
机构地区:[1]第四军医大学西京医院神经内科,西安710032
出 处:《神经解剖学杂志》2012年第6期554-560,共7页Chinese Journal of Neuroanatomy
摘 要:目的:研究人参皂甙Rd(Ginsenoside Rd,GSRd)对大鼠大脑中动脉栓塞(MCAO)模型损伤后,NMDA受体NR2B亚基的表达及其磷酸化的影响。方法:建立大鼠MCAO模型,并在术前及术后给予人参皂甙Rd,之后进行神经行为学评分,通过TTC(2,3,5-氯化三苯基四氮唑)染色观察脑梗死体积变化,采用Western blot方法检测脑缺血区不同时间点NR2B及其磷酸化的Ser1303及Tyr1472的表达情况。结果:GSRd能够改善大鼠神经行为学评分,减小模型大鼠脑梗死体积;MCAO模型大鼠脑缺血损伤处的NR2B亚基、磷酸化Ser1303及Tyr1472的表达量均较假手术组升高;在MCAO术前及术后给予GSRd,能够有效降低损伤侧NR2B亚基、磷酸化Ser1303及Tyr1472的表达量,并且GSRd对于上述各项表达量的影响呈剂量依赖性。结论:人参皂甙Rd能够有效降低MCAO模型中NR2B及磷酸化Ser1303及Tyr1472的水平,提示人参皂甙Rd可能是通过调节脑缺血再灌注损伤后NMDAR中NR2B亚基及该亚基磷酸化Ser1303、Tyr1472位点的水平,从而发挥其对脑缺血再灌注损伤的保护作用。Objective: To explore the effect of Ginsenoside Rd (GSRd) on NMDA receptor NR2B subunit and its phos- phorylation sites in rat middle cerebral artery occlusion (MCAO) model. Method: We first established rat MCAO model, and treated SD-rats with GSRd by intraperitoneal injection pre and after the MCAO operation; Second, to observe the effect of GSRd, we evaluated the differences of the ethology scores and the volume of cerebral infraction by TI'C staining between MCAO group and GSRd groups; In addition, we measured the expression of NR2B subunit and phosphorylation of NR2B subunit at Ser1303 and Tyr1472 sites by using Western blot. Results:GSRd significantly decreased the ethology scores and the volume of cerebral infraction, meanwhile, the results of Western blot analysis indicated that the expression of NR2B subunit and the phosphorylation of NR2B subunit at Serl303 and Tyr1472 in MCAO group remarkably in- creased, compared with sham operation group; Additionally, treated with GSRd pre or after MCAO operation, the expres- sion of NR2B subunit and the phosphorylation of NR2B subunit at Serl303 and Tyr1472 both decreased remarkably. Con- clusion:GSRd can reduce the expression of NR2B subunit and its phosphorylation level effectively in MCAO model, which suggests that decreasing the level of NR2B subunit and its phosphorylation level after ischemia injury may contribute to the neuroprotective mechanisms of GSRd.
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