Pathohistological and biochemical analysis in carotid plaque

一些报告表明脂质过氧化与人类颈动脉粥样硬化有关，然而，很少有报告表明人类颈动脉斑块与脂质过氧化之间存在联系。本研究探讨颈动脉内膜剥脱术(CEA)患者的临床特征、组织病理学特征、脂质过氧化与低密度脂蛋白(OxLDL)氧化的关系。CEA获得颈动脉/斑块。部分最严重的病变接受了组织病理学检查，其余的斑块进行了脂质过氧化和氧化低密度脂蛋白的检查。测定硫代巴比妥酸反应物质(TBARS)值作为脂质过氧化指标。用抗氧化型低密度脂蛋白(DLH3)和载脂蛋白B的特异性抗体用夹心ELISA法测定氧化型低密度脂蛋白的含量。用形态计量学方法测量斑块面积中富脂核(LC)和巨噬细胞浸润(MΦ)的百分比。根据检测结果，将所有斑块分为4组。第I组(GI)：Lg&lt；10%；组IIa(G1a)：LC 10-30%，MΦ&lt；5%；组IIb(GIIb)：LC 10-30%，MΦ[大于或等于]5%，以及组III(GIII)：LC[大于或等于]30%。牙周炎患者的斑块撕裂值显著高于牙周炎、牙周炎和牙周炎患者。在单个患者的配对样本中，氧化低密度脂蛋白斑块比血浆氧化低密度脂蛋白高近70倍(平均值±扫描电子显微镜，11.9±1.7vs0.18±0.01，p&lt；0.0001)。不稳定斑块的氧化低密度脂蛋白水平显著高于稳定斑块(19.6±2.8vs5.50±0.77，p&lt；0.0001)，且与斑块中DLH3抗原阳性相对应。不稳定斑块患者血浆OxLDL水平显著高于对照组(0.20±0.02vs0.13±0.01，P=0.02)。我们的结果表明，斑块和血浆中的TRARS和OxLDL可能是动脉粥样硬化易损性病变的预测指标。

Several reports have suggested an association between lipid peroxidation and human carotid atherosclerosis, however, few reports have demonstrated a link between lipid peroxidation and carotid plaques in humans. In this study, we investigated the relationship between clinical features, histopathological characteristics, lipid peroxidation and oxidation of low-density lipoprotein (OxLDL) in patients undergoing carotid endarterectomy (CEA). Carotid /plaques were obtained by CEA. A portion of the most severe lesions was subjected to histopathologic examination, and the remainder of the plaques examined for lipid peroxidation and OxLDL. Thiobarbituric acid-reactive substances (TBARS) values were determined as a marker for lipid peroxidation. Measurements of OxLDL were by sandwich ELISA using specific antibodies against OxLDL (DLH3) arid apoB. The lipid-rich core (LC) and macrophage infiltration (M Φ) component as a percentage of total plaque area were measured morphometrically. Based on the results, all plaques were classified into 4 groups. Group I (GI) : LG <10 % ; Group IIa (Glla) : LC 10-30 %, M Φ<5 % ; Group IIb (GIIb) : LC 10-30 %, M Φ【greater than or equal】5 %, and Group III (GIII) : LC 【greater than or equal】30 %. The plaque TEARS values of GUI were significantly higher than those of GI, GIIa, and GIIb. The TBARS values of GIIb were one-and-a-half times higher than those of Glla.In paired samples from individual patients, plaque OxLDL was nearly 70 times higher than plasma OxLDL (mean ± SEM, 11.9 ± 1.7 vs 0.18 ± 0.01, p<0.0001). The OxLDL level was significantly higher in unstable than stable plaques (19.6 ± 2.8 vs 5.50 ± 0.77, p<0.0001) and corresponded with DLH3 antigen positivity in the plaques. In patients with unstable plaques, plasma OxLDL was significantly higher than in the controls (0.20 ± 0.02 vs 0.13 ± 0.01, p=0.02). Our results suggest that TRARS and OxLDL in the plaque and plasma OxLDL may be a predictor of vulnerable atherosclerotic lesions.