水蛭提取物对大鼠脑血栓后脑组织MDA，SOD和NO含量的影响

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

Extract from hirudo protects ischemic brain tissues

AIM　To observe changes in contents of malondialdehyde (MDA), SOD and NO during photo-chemic ally induced thrombosis in the rat's brain, and to study mechanism of EFH in pro tection of its brain. METHODS　On cerebral thrombus designed model photo-chemically induced at the rat's middle cerebral artery, changes in contents of MDA, SOD and NO in brain homogenate were observed 4 h, 24 h after brain ischemia and drug action. RESULTS　At 4 h after the rat's brain ischemia M DA contents rose, and at 24 h rose significantly. At 24 h MDA contents in the hirudo treatment g roup dropped significantly from (4.77±0.24) mol*L-1 to (2.51±0.44) mol *L-1 (P<0.05). Compared with the model group at 24 h SOD activity significant ly r ose (P<0.05). At 4 h following ischemia NO contents dropped, and at 24 h rose significantly (P<0.05) compared with the pseudo-operation group. CONCLUSION　Brai n injury resulting from photo-chemically induced cerebral thrombus in the rat i s associated with neurocytotoxicity of MDA and NO. EFH blocks the production of M D A, reduces consumption of SOD, and weakens NO toxicity, thus providing protectio n for ischemic brain tissues.