CAJ | 학술논문

目的：研究开塞通对大鼠脑缺血损伤的保护作用。方法采用大脑中动脉线栓法建立脑缺血模型，缺血后检测脑组织中的丙二醛（ MDA）值、超氧化物歧化酶（ SOD）、ATP酶活性和细胞凋亡。结果缺血组MDA明显升高（P＜0．01），SOD、ATP酶活性明显降低（P＜0．01），细胞凋亡率显著升高。结论开塞通能清除氧自由基，减轻脂质过氧化反应，改善ATP 酶活性，抑制细胞凋亡从而减轻脑组织缺血损伤。
목적：연구개새통대대서뇌결혈손상적보호작용。방법채용대뇌중동맥선전법건립뇌결혈모형，결혈후검측뇌조직중적병이철（ MDA）치、초양화물기화매（ SOD）、ATP매활성화세포조망。결과결혈조MDA명현승고（P＜0．01），SOD、ATP매활성명현강저（P＜0．01），세포조망솔현저승고。결론개새통능청제양자유기，감경지질과양화반응，개선ATP 매활성，억제세포조망종이감경뇌조직결혈손상。
Objective To investigate the protective effect of Kai-sai-tong on focal cerebral ischemia in-jury in c rats.Methods A model of middle cerebral artery occlusion ( MCAO) in rats was established with in-traluminal filament occlusion.The malondialdehyde (MDA) content,superoxidedismutase (SOD) and ATPase activities and neuron apoptosis were detected after ischemia .Results Compared with control group ,MDA content and apoptosis rate were increased obviously (P<0.01) and SOD,ATPase activities were significantly reduced ( P<0 .01 ) in ischemia group .Compared with ischemia group ,Kai-sai-tong could markedly reduce MDA con-tent and apoptosis rate (P<0.01) and inprove SOD and ATPase activities (P<0.01).Conclusion Kai-sai-tong can scavenge oxygen radicals ,inhibit the reaction of lipidperoxidation ,improve SOD and ATPase activities and suppress neuron apoptosis .So Kai-sai-tong can decrease ischemic cerebral injury .