摘要
为探讨绞股蓝总皂甙抗缺血再灌注损伤的作用,本文检沿了大鼠海马结构缺血再灌注损伤后腺苷三磷酸(ATP)酶活性,并观察了病理组织学的改变.结果:缺血再灌注损伤后,海马结构组织Na^+—K^+—ATPase,Ca^(2+)—ATPase活性为12.56±0.81和24.83±0.55,较正常对照组(Na^+—K^+—ATPase16.07±1.42,Ca^(2+)—ATPase31.46±4.81)的活性明显下降(P<0.01).绞股蓝防治组Na^+—K^+—ATPase,Ca^(2+)—ATPase活性为15.58±2.12和29.61±1.31,脑活素防治组Na^+—K^+—AT-Pase,Ca^(2+)—ATPase活性为15.04±1.50和29.19±1.92,较缺血再灌注组明显上升(P<0.01).绞股蓝总皂甙防治组与脑活素防治组之间无明显差异(P>O.05).同时,海马1区神经毡损伤明显减轻.提示绞股蓝总皂甙有改善ATPase的功能,进而减轻缺血再灌注损伤后海马1区神经组织损害的功效.
In order to investigate the protective effect of Gynostemma pentaphyllum(GP) on the hippocampul formation ischemia reperfusion injury of rat. Tissue adenosine triphosphatase (ATPase)activity and histopathological changes in the hippocampal formatior were determined in the present study. Result: After ischemia-reperfusion injury,there was a significant decrease of ATPase activity(Na+-K+-ATPase 12. 56±0. 81,Ca2+-ATPase24. 83 ± 0. 55 VS Na + -K+ -ATPasel6. 07±1. 42, Ca2+-ATPase31- 46±4. 81)in control group (P<0. 01). In GP and Cere-brolysin (CL)treated group ,the increase of ATPase activityCGP Na+ -K+ -ATPase 15. 58±2.13.Ca2+-ATPase 29. 61±1.31. CL Na+-K+ -ATPase 15. 04±1.50,Ca2+-ATPase 29.19±1. 92) was significantly higher than that of ischemia reperfusion group(P<0. 01). The effect of GP group was similar to that of CL contral group. In addition,the neuronal damage observed under electronic microscope was also amelioraled substanlially. The results suggest that GP may provide the rapeutic protection in arresting neuronal damage in the hippocampai formation ischemia-reperfusion injury sa well sa improve ATPase activity.
出处
《咸宁医学院学报》
1996年第1期7-8,17,共3页
Journal of Xianning Medical College
