| Co-Investigator(Kenkyū-buntansha) |
ITABE Hiroyuki Tokyo University, Associate Professor, 薬学部, 助教授 (30203079)
FUKUZAWA Kenji The University of Tokushima, School of Medicine, Professor, 薬学部, 教授 (90035551)
NAGAHIRO Shinji The University of Tokushima, School of Medicine, Professor, 医学部, 教授 (60145315)
NISHI Kyoko The University of Tokushima, School of Medicine, Assistant, 医学部・附属病院, 助手 (60335817)
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| Research Abstract |
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.
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