Effects of complement C1q on motor function and postsynaptic density protein 95 of rats with cere-bral ischemia-reperfusion injury
- VernacularTitle: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
- Author:
Qingtong ZHANG
1
;
Chenyao JIAN
;
Mingda LIU
;
Shenquan CAI
;
Manlin DUAN
Author Information
- Keywords: Ischemia-reperfusion injury; Complement; Postsynaptic density protein 95; Motor dysfunction; Rat
- From: The Journal of Clinical Anesthesiology 2024;40(8):855-859
- CountryChina
- Language:Chinese
- Abstract: 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 ar-tery 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 subcom-ponent 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 signifi-cantly 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 shor-ter 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 com-plement therapy can effectively improve cerebral ischemia-reperfusion injury in rats.
