血管性痴呆小鼠海马线粒体复合体活性变化

目的:探讨血管性痴呆(VD)小鼠海马线粒体复合体活性变化。方法:抽取并回输约40%总血量加双侧颈总动脉夹闭20 min建立VD模型。病理学研究检测神经元损伤;分光光度计法检测丙二醛(MDA)含量、锰超氧化物歧化酶(Mn-SOD)活性和线粒体复合体活性;Western-blot检测Mn-SOD蛋白表达;Morris水迷宫评估学习记忆能力。结果:与假手术组相比,模型组学习记忆能力显著降低(P<0.05),MDA含量显著升高(P<0.05),Mn-SOD活性和蛋白表达显著降低(P<0.05);与假手术组相比,术后5 d模型组线粒体复合体Ⅰ、Ⅱ、Ⅲ、Ⅳ活性显著降低(P<0.05),术后15,30 d和60 d模型组线粒体复合体Ⅰ、Ⅱ活性无显著变化(P>0.05),复合体Ⅲ、Ⅳ活性显著降低(P<0.05);病理学检测显示模型组海马出现进行性神经元损伤。结论:线粒体复合体III、IV活性异常可能是VD的发病机制之一。

Changes of mitochondrial complex activity in vascular dementia mice

OBJECTIVE To investigate changes of mitochondrial complex activity in vascular dementia (VD) mice. METHODS VD model was established through drawing out and reperfusing 40% of whole blood volume plus clamping carotid arteries of mice for 20 min. Histological observation was performed to evaluate neural damage. Malonaldehyde (MDA), manganese superoxide dismutase (Mn-SOD) and mitochondrial complex activity were determined by using spectrophotometer. Expression of Mn-SOD was tested by western blot, learning and remembering ability were determined by Morris water maze. RESULTS Compared with sham operation group, MDA level was increased in I/R group (P<0.05). Activity and expression of Mn-SOD, learning and remembering ability were decreased in mice in model group (P<0.05). Activities of mitochondrial complex Ⅰ,Ⅱ, Ⅲ and Ⅳ in model group were lower than those in sham operation group in the 5 th day (P<0.05). In the 15th, 30 th and 60 th days, activities of complex Ⅲ and Ⅳ of model group were lower than those in sham operation group (P<0.05), but no significant difference was observed between model group and sham operation group in complex Ⅰ and Ⅱ activities (P>0.05). Progressive neural damages were observed in model group. CONCLUSION Abnormal activities of mitochondrial complex Ⅲ and Ⅳ may be involved in mechanisms of VD.