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目的:研究黄芪总苷和地卓西平马来酸(MK-801)对宫内窘迫后的缺氧后新生鼠的Tau蛋白磷酸化程度的影响。方法:采用2×3析因设计:即宫内窘迫(2水平:无处置、施行宫内窘迫即夹闭孕鼠的子宫动脉2/3持续10 min)和药物(3水平:生理盐水、MK-801、黄芪总苷)的所有组合。新生鼠生长至12周时留取海马,高效液相色谱(HPLC)检测谷氨酸(Glu)含量,IHC-SP检测p-AT8Ser202与GSK-3β1H8表达。结果:黄芪总苷可降低宫内窘迫诱发的Glu浓度升高;MK-801对海马中Glu的浓度无明显影响。宫内窘迫可增加海马内磷酸化程度的Tau蛋白p-AT8Ser202以及促进Tau蛋白磷酸化程度的调控蛋白GSK-3β1H8的表达;黄芪总苷和MK-801可减缓p-AT8~(Ser202)磷酸化程度。结论:黄芪总苷可以通过降低海马Glu浓度减缓Tau蛋白的磷酸化;GSK-3β是该信号通路的关键蛋白;黄芪总苷改善由于宫内窘迫诱发导致缺氧后的学习记忆能力低下的效果优于MK-801。
Objective: To study the effects of astragaloside and dextromethorphan maleate (MK-801) on Tau hyperphosphorylation in neonatal rats after intrauterine distress. METHODS: A 2 x 3 factorial design was used: intrauterine distress (2 levels: no treatment, intrauterine distress occlusion of the pregnant rat uterine artery for 2/3 for 10 min) and drug (3 levels: saline, MK -801, total astragaloside). The hippocampus of hippocampus was harvested at 12 weeks of gestation. Glu content was determined by high performance liquid chromatography (HPLC) and p-AT8Ser202 and GSK-3β1H8 by IHC-SP. Results: Astragalosides can reduce the intrauterine distress-induced increase in Glu concentration; MK-801 on Glu concentration in the hippocampus had no significant effect. Intrauterine distress can increase the phosphorylation of Tau protein p-AT8Ser202 in hippocampus and the expression of GSK-3β1H8, which regulates the phosphorylation of Tau protein. Astragalosides and MK-801 can slow the phosphorylation of p-AT8 ~ (Ser202) degree. Conclusion: Astragaloside can reduce the phosphorylation of Tau protein by decreasing the concentration of Glu in the hippocampus. GSK-3βis the key protein in the signal pathway. Astragaloside can improve the learning and memory abilities after hypoxia induced by intrauterine distress At MK-801.