CAJ | 학술논문

目的：通过检测局灶性脑缺血大鼠脑组织中NO含量的变化及左旋四氢巴马汀(L-tetrahydropalmatine,L-THP)的影响，从而探讨L-THP的脑保护作用机制。方法：采用线栓法制备大鼠右侧大脑中动脉阻断(MCAO)模型。应用硝酸还原酶法检测缺血3h及48h脑组织NO含量的变化及L-THP对NO含量的影响。结果：缺血3h及48h脑组织NO含量明显升高，且48h缺血组NO含量高于3h缺血组。缺血前30min应用L-THP20mg/kg可明显降低3h及48h脑缺血组织中NO含量。结论： L-THP可降低局灶性脑缺血脑组织中NO的含量。其脑保护作用是通过抑制NO介导的神经毒性作用实现的。
목적：통과검측국조성뇌결혈대서뇌조직중NO함량적변화급좌선사경파마정(L-tetrahydropalmatine,L-THP)적영향，종이탐토L-THP적뇌보호작용궤제。방법：채용선전법제비대서우측대뇌중동맥조단(MCAO)모형。응용초산환원매법검측결혈3h급48h뇌조직NO함량적변화급L-THP대NO함량적영향。결과：결혈3h급48h뇌조직NO함량명현승고，차48h결혈조NO함량고우3h결혈조。결혈전30min응용L-THP20mg/kg가명현강저3h급48h뇌결혈조직중NO함량。결론： L-THP가강저국조성뇌결혈뇌조직중NO적함량。기뇌보호작용시통과억제NO개도적신경독성작용실현적。
Objective：To measure the change of nitric oxide (NO) content in focal ischemic cerebral tissue of rats and the influence of L-THP, and to explore the mechanism of protective effect of L-THP. Methods: Cerebral ischemia was achieved by occluding the middle cerebral artery with an intraluminal suture technique in rats. The change of NO content in 3 hours and 48 hours ischemic cerebral tissue and the influence of L-THP was measured by nitrate redutase method. Results:NO content in 3 hours and 48 hours ischemic cerbral tissue was significantly increased, and the group of 48 hours ischemia was higher than 3 hours group. L-THP treated 30 minutes before cerebral ischemia can significantly decrease NO content in ischemic cerebral tissue. Conclusion: L-THP could decrease NO content in focal ischemic cerebral tissue. The mechanism of neuroprotective effect of L-THP was by inhibiting the neurotoxicity of NO-mediated.