Pathohistological and biochemical analysis in carotid plaque

一些报告已经表明脂质过氧化和人类颈动脉粥样硬化之间的关联，然而，很少有报告表明脂质过氧化和人类颈动脉斑块之间的联系。在这项研究中，我们研究了颈动脉内膜切除术（CEA）患者的临床特征，组织病理学特征，脂质过氧化和低密度脂蛋白（OxLDL）氧化之间的关系。颈动脉/斑块通过CEA获得。对最严重病变的一部分进行组织病理学检查，并对斑块的其余部分进行脂质过氧化和OxLDL检查。硫代巴比妥酸反应物质（TBARS）值被确定为脂质过氧化的标志物。通过使用针对OxLDL（DLH 3）和apoB的特异性抗体的夹心ELISA测量OxLDL。通过形态计量学测量富脂核心（LC）和巨噬细胞浸润（M Φ）组分占总斑块面积的百分比。根据结果，将所有斑块分为4组。第I组（GI）：LG <10%; IIa组（Glla）：LC 10- 30%，M Φ<5%; IIb组（GIIb）：LC 10- 30%，M Φ[大于或等于] 5%，III组（GIII）：LC [大于或等于] 30%。GUI的斑块TEARS值显著高于GI、GIIa和GIIb。GIIb的TBARS值是Glla的1.5倍。在个体患者的配对样本中，斑块OxLDL比血浆OxLDL高近70倍（平均值± SEM，11.9 ± 1.7 vs 0.18 ± 0.01，p<0.0001）。不稳定斑块中OxLDL水平显著高于稳定斑块（19.6 ± 2.8 vs 5.50 ± 0.77，p<0.0001），并且与斑块中DLH 3抗原阳性相对应。在不稳定斑块患者中，血浆OxLDL显著高于对照组（0.20 ± 0.02 vs 0.13 ± 0.01，p=0.02）。我们的研究结果表明，斑块和血浆中的TRARS和OxLDL可能是易损性动脉粥样硬化病变的预测因子。

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.