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目的探讨脑血管疾病患者血清中白细胞介素33(IL-33)水平与颈动脉粥样硬化斑块稳定性及脑梗死的关系及其作用机制。方法采用ELISA方法检测脑梗死组(n=63)、短暂性脑缺血发作组(n=30)及正常对照组(n=15)血清中IL-33的表达水平;采用Western blotting、荧光定量PCR(qRT-PCR)和ELISA法检测体外培养的人外周血单个核细胞(PBMC)和U937细胞在接受外源性IL-33刺激后,MMP-9和Cox-2的表达量变化。结果脑梗死组IL-33的表达水平低于对照组和短暂性脑缺血发作组(P均<0.01);脑梗死组中不稳定斑块、稳定斑块和无斑块患者血清中IL-33的表达水平逐渐降低(P<0.01);脑梗死组中,与无糖尿病和高血脂症的患者相比,合并糖尿病和高脂血症的患者血清中IL-33水平降低(P均<0.01);外源性IL-33刺激可下调外周血单核细胞和U937细胞中M M P-9和Cox-2的表达和分泌量。结论 IL-33可被作为预测脑梗死及不稳定性粥样硬化斑块的潜在的血清标志物和治疗靶点。
Objective To investigate the relationship between the level of interleukin-33 (IL-33), the stability of carotid atherosclerosis plaque and cerebral infarction in patients with cerebrovascular diseases and its mechanism. Methods The serum levels of IL-33 in cerebral infarction group (n = 63), transient ischemic attack group (n = 30) and normal control group (n = 15) were detected by ELISA. The expression of MMP-9 and Cox-2 in human peripheral blood mononuclear cells (PBMCs) and U937 cells stimulated by exogenous IL-33 were detected by qRT-PCR and ELISA. Results The level of IL-33 in cerebral infarction group was lower than that in control group and transient ischemic attack group (all P <0.01). In the cerebral infarction group, the level of IL- (P <0.01). Compared with patients without diabetes and hyperlipidemia, the levels of IL-33 in serum of patients with diabetes mellitus and hyperlipidemia were lower than those without diabetes (P <0.01) ); Exogenous IL-33 stimulation can down-regulate the expression and secretion of MM P-9 and Cox-2 in peripheral blood mononuclear cells and U937 cells. Conclusion IL-33 can be used as a potential serum marker and therapeutic target for predicting cerebral infarction and unstable atherosclerotic plaques.