Pitavastatin Reduces Lectin-Like Oxidized Low-Density Lipoprotein Receptor-1 Ligands in Hypercholesterolemic Humans

Pitavastatin Reduces Lectin-Like Oxidized Low-Density Lipoprotein Receptor-1 Ligands in Hypercholesterolemic Humans
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DOI:
10.1007/s11745-010-3402-7
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发表时间:
2010-03
期刊:
影响因子:
1.9
通讯作者:
Tetsuya Matsumoto;M. Fujita;T. Sawamura;A. Kakino;Yuko Sato;Y. Fujita;H. Matsuda;M. Nakanishi;K. Uchida;I. Nakae;H. Kanda;Akira Yoshida;K. Miwa;H. Hayashi;K. Mitsunami;M. Horie
Tetsuya Matsumoto;M. Fujita;T. Sawamura;A. Kakino;Yuko Sato;Y. Fujita;H. Matsuda;M. Nakanishi;K. Uchida;I. Nakae;H. Kanda;Akira Yoshida;K. Miwa;H. Hayashi;K. Mitsunami;M. Horie
中科院分区:
医学4区
文献类型:
--
作者:
Tetsuya Matsumoto;M. Fujita;T. Sawamura;A. Kakino;Yuko Sato;Y. Fujita;H. Matsuda;M. Nakanishi;K. Uchida;I. Nakae;H. Kanda;Akira Yoshida;K. Miwa;H. Hayashi;K. Mitsunami;M. Horie

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本研究的目的是确定匹伐他汀对高胆固醇血症患者低密度脂蛋白胆固醇(LDL-C)和凝集素样氧化LDL受体-1(LOX-1)的影响。检查了25例未接受抗血脂异常药物治疗且LDL-C水平超过160 mg/dL的高胆固醇血症患者(8例男性,17例女性;年龄66 ± 13,21-80岁)。在基线和匹伐他汀(2 mg/d)治疗6个月后测量生化因子。用ELISA法测定血清LOX-1与载脂蛋白B-100颗粒配体和可溶性LOX-1(sLOX-1)的水平。所有受试者均完成了研究,无不良副作用。总胆固醇(268 ± 26 vs. 176 ± 17 mg/dL)、LDL-C(182 ± 21 vs. 96 ± 14 mg/dL)和LOX-1配体(867 ± 452 vs. 435 ± 262 ng/mL)在匹伐他汀治疗后降低(各P< 0.0001)。三酰甘油显著降低(P< 0.0001),但高密度脂蛋白胆固醇无变化。6个月后,高敏CRP或可溶性LOX-1无显著变化。基线时,LOX-1配体与LDL-C或sLOX-1之间无显著相关性。LOX-1配体的降低与LDL-C的降低不相关,但与sLOX-1的降低相关(r= 0.47,P < 0.05)。总之,匹伐他汀治疗对高胆固醇血症受试者的氧化应激标志物具有有益作用。血清LOX-1配体水平可能是他汀类药物多效性作用的有用生物标志物。
The aim of this study was to determine the impact of pitavastatin on low-density lipoprotein cholesterol (LDL-C) and lectin-like oxidized LDL receptor-1 (LOX-1) in patients with hypercholesterolemia. Twenty-five hypercholesterolemic patients (8 male, 17 female; age 66 ± 13, 21–80 years) who had not received anti-dyslipidemic agents and had LDL-C levels of more than 160 mg/dL were examined. Biochemical factors were measured at baseline and after treatment with pitavastatin (2 mg/day) for 6 months. Serum levels of LOX-1 with apolipoprotein B-100 particle ligand and a soluble form of LOX-1 (sLOX-1) were measured by ELISA. All subjects completed the study with no adverse side effects. Total-C (268 ± 26 vs. 176 ± 17 mg/dL), LDL-C (182 ± 21 vs. 96 ± 14 mg/dL), and LOX-1 ligand (867 ± 452 vs. 435 ± 262 ng/mL) were reduced with pitavastatin treatment (P< 0.0001 for each). Significant decreases in triacylglycerols were noted (P< 0.0001), but there were no changes in high-density lipoprotein cholesterol. After 6 months, there were no significant changes in high-sensitivity CRP or soluble LOX-1. At baseline, there were no significant correlations between LOX-1 ligand and either LDL-C or sLOX-1. The decrease in LOX-1 ligand was not correlated with the decrease in LDL-C, but was correlated with the decrease in sLOX-1 (r= 0.47,P< 0.05). In conclusion, pitavastatin therapy had beneficial effects on markers of oxidative stress in hypercholesterolemic subjects. Serum levels of LOX-1 ligand may be a useful biomarker of the pleiotropic effects of statins.