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| 补体C1q对脑缺血-再灌注损伤大鼠运动功能和突触蛋白PSD95的影响 |
| Effects of complement C1q on motor function and postsynaptic density protein 95 of rats with cerebral ischemia-reperfusion injury |
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| DOI：10.12089/jca.2024.08.013 |
| 中文关键词: 缺血-再灌注损伤 补体 突触后密度蛋白95 运动功能障碍 大鼠 |
| 英文关键词: Ischemia-reperfusion injury Complement Postsynaptic density protein 95 Motor dysfunction Rat |
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| 中文摘要: |
目的：探讨补体C1q对脑缺血-再灌注损伤大鼠运动功能和突触后密度蛋白95（PSD95）的影响。
方法：选择清洁级雄性SD大鼠36只，6～8周龄，体重220～250 g。采用随机数字表法将大鼠分为三组：假手术组（S组）、大脑中动脉栓塞（MCAO）组（M组）和MCAO+C1q中和抗体组（A组），每组12只。S组大鼠仅接受颈总动脉解剖分离，不置入线栓；M组采用线栓法制备MCAO大鼠模型；A组在大鼠建模后1 d通过侧脑室注射C1q中和抗体10 μl。建模后3 d通过黏附去除实验记录黏附刺激去除时间，通过平衡木实验评估大鼠肢体运动功能，处死大鼠后采用ELISA法检测海马组织C1q、C3含量，采用Western blot法检测海马组织C1q子成分亚基A（C1qa）和PSD95蛋白含量，采用尼氏染色记录尼氏小体数量。
结果：与S组比较，M组黏附刺激去除时间明显延长，平衡木实验评分明显升高，海马组织C1q、C3含量、C1qa蛋白含量明显升高，PSD95蛋白含量明显降低，尼氏小体数量明显减少（P<0.05）。与M组比较，A组黏附刺激去除时间明显缩短，平衡木实验评分明显降低，海马组织C1q、C3含量、C1qa蛋白含量明显降低，PSD95蛋白含量明显升高，尼氏小体数量明显增加（P<0.05）。
结论：大鼠脑缺血-再灌注损伤可诱发补体系统广泛激活，并通过补体蛋白C1q加重大鼠海马组织突触蛋白PSD95的丢失及运动功能障碍；中和补体疗法可有效改善大鼠脑缺血-再灌注损伤。 |
| 英文摘要: |
Objective: To explore the effects of complement C1q on postsynaptic density protein 95 (PSD95) and motor function of rats with cerebral ischemia-reperfusion injury.
Methods: Thirty-six clean male SD rats, aged 6-8 weeks, weighing 220-250 g, were randomly divided into three groups: sham group (group S), middle cerebral artery occlusion (MCAO) group (group M), and MCAO + C1q neutralization group (group A), 12 rats in each group. Group S only received anatomical separation of common carotid artery without insertion of monofilament, group M established the MCAO model was prepared by insertion of monofilament, and group A received C1q neutralizing antibody 10 μl injected into the lateral ventricle on the first day after establishing MCAO model. Three days after modeling, the adhesion removal experiment was used to record the adhesion stimulus removal time, and the balance beam experiment was used to evaluate the limb motor function of the rats. After the rats were sacrificed, the ELISA method was used to detect the C1q and C3 levels in the hippocampus tissue, the Western blot method was used to detect the C1q subcomponent subunit A (C1qa) and PSD95 protein levels in the hippocampus tissue, and the Nissl staining was used to record the number of Nissl bodies.
Results: Compared with group S, group M exhibited a significantly longer adhesion removal time, significantly elevated balance beam experiment score, significantly higher levels of C1q, C3, and C1qa in the hippocampus, and significantly lower levels of PSD95 and Nissl's body count in the hippocampus (P < 0.05). Compared with group M, group A exhibited significantly shorter adhesion removals, a significantly lower balance beam experiment score, significantly lower levels of C1q, C3, and C1qa in the hippocampus, significantly higher PSD95 content, and a significantly higher Nissl's body count in the hippocampus (P < 0.05).
Conclusion: Cerebral ischemia-reperfusion injury in rats can induce extensive activation of the complement system and aggravate the loss of synaptic protein PSD95 and motor dysfunction in rat hippocampal tissue through complement protein C1q. Neutralizing complement therapy can effectively improve cerebral ischemia-reperfusion injury in rats. |
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