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Kinin B1 receptor as a novel prognostic progression biomarker for carotid atherosclerotic plaques

机译:激肽B1受体作为一种新的颈动脉粥样硬化斑块的预后生物标志物

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摘要

Stroke caused by atherosclerosis remains a leading cause of morbidity and mortality worldwide, associated with carotid plaque rupture and inflammation progression. However, the inflammatory biomarkers which aid in predicting the future course of plaques are less detailed. The present study investigated the association between plaque vulnerable and inflammatory biomarkers using blood and plaque specimens. Carotid plaque specimens were obtained from 80 patients following stroke, 14 patients suffering from transient ischaemic attack and 17 asymptomatic patients that underwent carotid endarterectomy. To assess changes in plaque characteristics at histological levels, plaques were categorized by the time between the latest ischemic stroke and surgical intervention within 30, 30–90, 90–180 and over 180 days following stroke. Serum levels of inflammatory biomarkers interleukin (IL)-6, IL-10 and kinin B1 receptor (B1R) were measured by ELISA. Histological assessment of plaque was used to evaluate the plaque stability, progression and the inflammatory biomarker levels. Comparisons of histological characteristics demonstrated that plaques revealed an unstable phenotype following stroke within 30, 30–90 days and then remodeled into more stable plaques following stroke at 90–180 and over 180 days. By comparing the serum levels of inflammatory biomarkers, it was observed that IL-6 and B1R levels tended to decline whereas IL-10 levels increased in stroke patients from <30 days to over 180 days. Immunohistochemical analysis of IL-6, IL-10 and B1R demonstrated similar alterations in serum levels. Correlation analyses revealed that only B1R serum level was significantly correlated with histological level in patients with carotid atherosclerosis. The findings revealed that serum B1R levels may provide prognostic information and currently act as potential indicators for progression in atherosclerosis.
机译:由动脉粥样硬化引起的中风仍然是全世界发病率和死亡率的主要原因,与颈动脉斑块破裂和炎症进展有关。然而,有助于预测斑块未来病程的炎性生物标志物较不详尽。本研究使用血液和斑块标本调查了易损斑块和炎症生物标记之间的关联。从中风后的80例患者,14例经历短暂性脑缺血发作的患者和17例接受颈动脉内膜切除术的无症状患者获得了颈动脉斑块标本。为了在组织学水平上评估斑块特征的变化,按照在卒中后30、30-90、90-180和180天内最新的缺血性卒中与手术干预之间的时间对斑块进行分类。通过ELISA测量血清中炎性生物标志物白介素(IL)-6,IL-10和激肽B1受体(B1R)的水平。斑块的组织学评估用于评估斑块的稳定性,进展和炎性生物标志物水平。组织学特征的比较表明,斑块在卒中后30、30-90天内显示出不稳定的表型,然后在卒中后90-180和180天内重构为更稳定的斑块。通过比较血清中炎性生物标志物的水平,观察到中风患者的IL-6和B1R水平趋于下降,而IL-10水平则从30天到180天以上升高。 IL-6,IL-10和B1R的免疫组织化学分析显示血清水平也有类似变化。相关分析显示,颈动脉粥样硬化患者中只有B1R血清水平与组织学水平显着相关。研究结果表明,血清B1R水平可能提供预后信息,目前可作为动脉粥样硬化进展的潜在指标。

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