水蛭提取物对大鼠脑血栓后脑组织MDA，SOD和NO含量的影响

摘要

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4 h，24 h脑组织匀浆中MDA，SOD和NO的含量变化. 结果　大鼠脑缺血后4 h 时MDA的含量增高，24 h明显增高；24 h时EFH治疗组 MDA含量明显降低，由(4.77±0.24) mol*L-1降为(2.51±0.44) mol*L-1 (P<0.05)，与模 型组相比24 h时SOD的活性明显增高(P<0.05). NO含量在脑缺血后4 h降低，24 h时与 假 手术组相比明显升高(P<0.01). 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.%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.