血清ZO-1、aβ2-GP水平与脑梗死患者梗死病灶范围及颈动脉粥样硬化程度的相关性

Correlation of serum ZO-1 and aβ2-GP levels with infarct lesion extent and degree of carotid atherosclerosis in patients with cerebral infarction

目的探讨血清闭锁小带蛋白1(ZO-1)、抗β2糖蛋白1抗体(aβ2-GP1)水平与脑梗死患者梗死病灶范围及颈动脉粥样硬化程度的相关性。方法选取2020年1月至2023年1月于保定市第一中心医院进行治疗的脑梗死患者103例作为研究组,另选取同期该院的体检健康者51例作为对照组。依据梗死病灶范围将脑梗死患者分为大梗死组(梗死病灶>50 cm 2),中梗死组(梗死病灶在10~50 cm 2),小梗死组(梗死病灶<10 cm 2)。依据颈动脉彩超结果将脑梗死患者分为斑块期组、增厚期组、管壁正常组。采用酶联免疫吸附试验检测血清ZO-1、aβ2-GP1水平,并比较各组ZO-1、aβ2-GP1水平变化;采用Spearman相关分析脑梗死患者血清ZO-1、aβ2-GP1水平与梗死病灶范围及颈动脉粥样硬化程度的相关性。结果研究组血清ZO-1水平低于对照组,血清aβ2-GP1水平高于对照组(P<0.05)。在103例脑梗死患者中,大梗死组有32例,中梗死组有34例,小梗死组有37例,其中小梗死组ZO-1水平高于中梗死组和大梗死组,aβ2-GP1水平低于中梗死组和大梗死组(P<0.05);中梗死组ZO-1水平高于大梗死组,aβ2-GP1水平低于大梗死组(P<0.05)。在103例脑梗死患者中,斑块期组有29例,增厚期组有38例,管壁正常组有36例,其中斑块期组血清ZO-1水平低于增厚期组和管壁正常组,aβ2-GP1水平高于增厚期组和管壁正常组(P<0.05);增厚期组血清ZO-1水平低于管壁正常组,aβ2-GP1水平高于管壁正常组(P<0.05)。Spearman相关分析发现,脑梗死患者血清ZO-1水平与颈动脉粥样硬化程度和梗死病灶范围呈负相关(P<0.05),aβ2-GP1水平与颈动脉粥样硬化程度和梗死病灶范围呈正相关(P<0.05)。结论脑梗死患者血清ZO-1和aβ2-GP1水平与颈动脉粥样硬化程度和梗死病灶范围有着明显的相关性,在脑梗死患者的病情诊断、治疗和预后中具有潜在价值。

Objective To investigate the correlation of serum atresia zonule protein 1(ZO-1)and anti-β2-glycoprotein 1 antibody(aβ2-GP1)levels with infarct lesion extent and degree of carotid atherosclerosis in patients with cerebral infarction.Methods A total of 103 patients with cerebral infarction treated in Baoding No.1 Central Hospital from January 2020 to January 2023 were selected as the study group,and 51 healthy subjects in the same hospital during the same period were selected as the control group.Patients with cerebral infarction were divided into large infarction group(infarct lesion extent>50 cm 2),middle infarction group(infarct lesion extent as 10-50 cm 2),and small infarction group(infarct lesion extent<10 cm 2)according to the infarct lesion extent.According to the results of carotid ultrasound,the patients with cerebral infarction were divided into plaque stage group,thickening stage group and normal vessel wall group.Enzyme-linked immunosorbent assay was used to detect serum ZO-1,aβ2-GP1 levels,and the levels of ZO-1 and aβ2-GP1 in each group were compared.Spearman correlation analysis was used to analyze the correlation between serum ZO-1,aβ2-GP1 levels and the infarct lesion extent and the degree of carotid atherosclerosis in patients with cerebral infarction.Results The study group had a significantly lower serum level of ZO-1 and a significantly higher serum level of aβ2-GP1 than the control group(P<0.05).Among the 103 patients with cerebral infarction,there were 32 cases in the large infarction group,34 cases in the middle infarction group,and 37 cases in the small infarction group.The small infarction group had a significantly higher level of ZO-1 and a significantly lower level of aβ2-GP1 than the medium infarction group and large infarction group(P<0.05).The middle infarction group had a significantly higher level of ZO-1 and a significantly lower level of aβ2-GP1 than the large infarction group(P<0.05).Among 103 patients with cerebral infarction,there were 29 cases in the plaque stage group,38 cases in the thickening stage group,6 cases in the normal vessel wall group.The plaque stage group had a significantly lower serum level of serum ZO-1 and a significantly higher level of aβ2-GP1 than the thickening stage group and normal vessel wall group(P<0.05).The thickening stage group had a significantly lower serum level of ZO-1 and a significantly higher serum level of aβ2-GP1 than the normal vessel wall group(P<0.05).Spearman correlation analysis showed that the serum level of ZO-1 was negatively correlated with the degree of carotid atherosclerosis and the extent of infarction(P<0.05),and the serum level of aβ2-GP1 was positively correlated with the degree of carotid atherosclerosis and the extent of infarction(P<0.05).Conclusion The levels of serum ZO-1 and aβ2-GP1 in patients with cerebral infarction are significantly correlated with the degree of carotid atherosclerosis and the extent of infarction,which have potential value in the diagnosis,treatment and prognosis of patients with cerebral infarction.