Objective: To determine the protective effect of monosialoganglionside (GM1) and evaluate the influence of GM1 on expression of N-methyl-D-aspartate receptor subunit 1 (NMDAR1) in Sprague-Dawley (SD) rats with focal c...Objective: To determine the protective effect of monosialoganglionside (GM1) and evaluate the influence of GM1 on expression of N-methyl-D-aspartate receptor subunit 1 (NMDAR1) in Sprague-Dawley (SD) rats with focal cerebral ische- mia-reperfusion (I/R). Methods: Left middle cerebral artery (MCA) was occluded by an intraluminal suture for 1 h and the brain was reperfused for 72 h in SD rats when infarct volume was measured, GM1 (10 mg/kg) was given ip (intraperitoneally) at 5 min (group A), 1 h (group B) and 2 h (group C) after MCA occlusion (MCAo). Expression of NMDAR1 was detected by Western blot at various time after reperfusion (4 h, 6 h, 24 h, 48 h and 72 h) in ischemic hemispheres of the rats with or without GM1 admin- istered. Results: (1) Adjusted relative infarct volumes of groups A and B were significantly smaller than that of group C and the control group (P<0.01 and P<0.05, respectively). (2) Expression level of NMDAR1 was temporally high at 6 h after reperfusion, and dipped below the normal level at 72 h after reperfusion. GM1 at 5 min after MCAo significantly suppressed the expression of NMDAR1 at 6 h after reperfusion (P<0.05 vs the control). At 72 h after reperfusion, the NMDAR1 expression level of rats treated with GM1 administered (at 5 min or 2 h after MCAo) was significantly higher than that of the control (P<0.05). Conclusion: GM1 can time-dependently reduce infarct volume in rats with focal cerebral I/R partly through stabilizing the expression of NMDAR1.展开更多
文摘目的:观察内环境因素(pH和甘氨酸及离子浓度)对依达拉奉抗神经元缺血性损伤作用的影响。方法:大鼠原代培养皮质神经元,在不同的实验溶液(模拟缺血后脑内环境的变化)以缺氧缺糖(oxygen-g lucose deprivation,OGD)3 h和再灌12 h诱导皮质神经元损伤,以噻唑蓝(MTT)还原反应和乳酸脱氢酶(LDH)释放观察损伤变化。观察不同实验溶液对抗脑缺血药物依达拉奉抗缺血性损伤作用的影响。结果:在弱碱性(pH 7.8)或含甘氨酸(10μm o l/L)的实验溶液中,OGD损伤加重;在弱酸性(pH 6.5)或高M g2+(1.8 mm o l/L)条件下,OGD损伤减轻。依达拉奉(1μm o l/L)能逆转在pH 6.1、7.4、7.8或含甘氨酸溶液中OGD损伤;而对pH 6.5、高M g2+或低Ca2+溶液中的OGD损伤未显示保护作用。结论:内环境因素改变可影响缺血性损伤程度和依达拉奉抗损伤作用。
基金Project (No. 2004QN012) supported by the Youth Talent SpecialFund of Health Bureau of Zhejiang Province the National BasicResearch Program (973) of China (No. G1999054000) and the Na-tional Natural Science Foundation of China (No. 30371637)
文摘Objective: To determine the protective effect of monosialoganglionside (GM1) and evaluate the influence of GM1 on expression of N-methyl-D-aspartate receptor subunit 1 (NMDAR1) in Sprague-Dawley (SD) rats with focal cerebral ische- mia-reperfusion (I/R). Methods: Left middle cerebral artery (MCA) was occluded by an intraluminal suture for 1 h and the brain was reperfused for 72 h in SD rats when infarct volume was measured, GM1 (10 mg/kg) was given ip (intraperitoneally) at 5 min (group A), 1 h (group B) and 2 h (group C) after MCA occlusion (MCAo). Expression of NMDAR1 was detected by Western blot at various time after reperfusion (4 h, 6 h, 24 h, 48 h and 72 h) in ischemic hemispheres of the rats with or without GM1 admin- istered. Results: (1) Adjusted relative infarct volumes of groups A and B were significantly smaller than that of group C and the control group (P<0.01 and P<0.05, respectively). (2) Expression level of NMDAR1 was temporally high at 6 h after reperfusion, and dipped below the normal level at 72 h after reperfusion. GM1 at 5 min after MCAo significantly suppressed the expression of NMDAR1 at 6 h after reperfusion (P<0.05 vs the control). At 72 h after reperfusion, the NMDAR1 expression level of rats treated with GM1 administered (at 5 min or 2 h after MCAo) was significantly higher than that of the control (P<0.05). Conclusion: GM1 can time-dependently reduce infarct volume in rats with focal cerebral I/R partly through stabilizing the expression of NMDAR1.
