摘要
目的 观察内抑素基因对动脉粥样硬化斑块发展的作用。方法 采用重组内抑素基因的真核表达载体 ,对不同周龄的ApoE基因敲除的动脉粥样硬化小鼠进行电脉冲介导的骨骼肌内抑素基因转移 ,共进行 10次基因转移 ,以空载质粒作为对照。结果 2 4周龄组处理前主动脉起始部狭窄率为 16 %± 4% ,经过 2 0周处理后对照组平均狭窄率为 5 6 %± 14% ,治疗组为 34 %± 8% ,较对照组减轻了 5 4%。 36周龄组处理前平均狭窄率为 30 %± 6 % ,2 0周处理后对照组为 6 4%± 12 % ,治疗组为49 %± 10 % ,较对照组减轻了 44 %。治疗组斑块内内皮细胞数和毛细血管出现率较对照组均减少 ,两组间血脂指标没有差异。
Objective To investigate the effect of endostatin gene transfer mediated by electric pulses into skeletal muscles of mice upon the develpment of atherosclerotic plaques. Methods Eukaryotic expression plasmid of mouse endostatin was injected into the muscles of 2 groups of ApoE deficient mice, group A at the age of 24 weeks, and group B at the age of 36 weeks (named therapy group as a whole). Gene transfer was mediated by electric pulses for ten times. Empty plasmid was used to mice at the same ages as controls. Twenty weeks later, blood lipid was tested, and the aortas of the experimental animals were taken out to examine the areas of atherosclerotic plaques and count the endothelial cells and microvessels in the plaques. Results In the 24 week aged group, the stenosis rate of aorta 16%±4% before the experiment. Twenty weeks later, the stenosis rate was 56%±14% among the control mice, and was 34%±8% among the treated ones with an improvement rate of 54%. In the 36 week aged group, the stenosis rate of aorta was 30%±6% before the experiment. Twenty weeks after the begining of experiment, the stenosis rate was 64%±12% among the control mice, and was 49%±10% among the treated ones with an improvement rate of 44%. Twenty weeks after the begining of experiment, the endothelial cell count and microvessel appearance rate were less among the therapy group than among the controls. There was no significant difference in blood lipid between the therapy group and the control group. Conclusion Endostatin gene transfer into skeletal muscle effectively inhibits the development of atherosclerotic plaques.
出处
《中华医学杂志》
CAS
CSCD
北大核心
2001年第12期726-729,共4页
National Medical Journal of China
