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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 investigate the effect of ginsenoside Rd (GSRd) on the expression of NR2B subunit of NMDA receptor and its phosphorylation after MCAO injury in rats. Methods: Rat model of MCAO was established. Ginsenoside Rd was given before and after operation. Neurobehavioral score was then used. The volume of cerebral infarction was observed by TTC (2,3,5,5-trichlorotoluene tetrachloride) staining Western blot was used to detect the expression of NR2B, phosphorylated Ser1303 and Tyr1472 at different time points after cerebral ischemia. Results: GSRd improved neurobehavioral scores and decreased cerebral infarct volume in rats. The expression of NR2B subunit, phosphorylated Ser1303 and Tyr1472 in MCAO model rats were higher than those in sham-operation group . The administration of GSRd before and after MCAO can effectively reduce the expression of NR2B subunit, phosphorylated Ser1303 and Tyr1472 on the injured side, and the effect of GSRd on the above expression is dose-dependent. CONCLUSION: Ginsenoside Rd can effectively decrease the levels of NR2B, phosphorylated Ser1303 and Tyr1472 in MCAO model, suggesting that ginsenoside Rd may be mediated by regulating NR2B subunit of NMDAR and phosphorylation of Ser1303, Tyr1472 in NMDAR after cerebral ischemia-reperfusion injury Site level, which play its role in cerebral ischemia-reperfusion injury.