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目的 探讨光化学法诱导大鼠脑血栓形成中丙二醛(MDA) ,NO和 SOD含量的变化及水蛭提取物 (EFH )对其脑组织保护作用的机理 .方法 采用光化学法诱导大鼠大脑中动脉 (MCA)脑血栓形成模型 ,观察脑缺血后及药物作用后 4h,2 4h脑组织匀浆中 MDA,SOD和 NO的含量变化 .结果 大鼠脑缺血后 4h时 MDA的含量增高 ,2 4h明显增高 ;2 4h时 EFH治疗组 MDA含量明显降低 ,由 (4 .77± 0 .2 4) mol·L- 1降为 (2 .5 1± 0 .44 ) mol· L- 1 (P<0 .0 5 ) ,与模型组相比2 4h时 SOD的活性明显增高 (P<0 .0 5 ) . NO含量在脑缺血后 4h降低 ,2 4h时与假手术组相比明显升高 (P<0 .0 1) .结论 光化学诱导大鼠脑血栓形成 ,其脑组织的损伤与 MDA及 NO的神经细胞毒性作用有关 ,EFH可清除 MDA的生成 ,减少 SOD消耗 ,降低 NO的毒性 ,对缺血脑组织有保护作用
Objective To investigate the changes of malondialdehyde (MDA), NO and SOD levels induced by photochemical method in rat cerebral thrombosis and the protective mechanism of leech extract (EFH) on brain tissue. Methods Photochemical method was used to induce middle cerebral artery in rats. (MCA) Cerebral thrombosis model was used to observe the content of MDA, SOD and NO in brain homogenate after cerebral ischemia and 4h, 24h after drug action. Results The content of MDA increased 4h after cerebral ischemia in rats. 2 At 4h, the MDA content in the EFH treatment group was significantly decreased from (4.77±0.24) mol·L-1 to (2.51±0.44) mol·L-1(P). <0. 0 5) Compared with the model group, the activity of SOD was significantly higher at 24 hours (P<0.05). The content of NO decreased 4 hours after cerebral ischemia, and it was significantly increased at 24 hours compared with the sham group. High (P<0.01). Conclusion Photochemically induced cerebral thrombosis in rats, and its brain tissue damage is related to the neurotoxicity of MDA and NO. EFH can eliminate MDA production, reduce SOD consumption, and reduce the toxicity of NO. , Protective effect on ischemic brain tissue