低密度脂蛋白分泌后修饰,单细胞功能和循环粘附分子在2型糖尿病患者和没有大血管并发症的2型糖尿病患者:阿尔法-托科菲罗尔补充剂的效果
1Division of Clinical Biochemistry and Human Metabolism, Department of Pathology, University of Texas Southwestern Medical Center, Dallas 75235-9073, USA.
Circulation
|July 13, 2000
概括
这项研究表明,2型糖尿病会增加单细胞活动和粘附,而不考虑宏血管疾病. 在糖尿病患者中,RRR-alpha-tocopherol疗法有效地降低了这些益动脉增生效应.
科学领域:
- 心血管研究研究心血管研究
- 内分泌学 在内分泌学.
- 免疫学 免疫学 免疫学
背景情况:
- 糖尿病会加速动脉样硬化.
- 在有或没有宏血管疾病的2型糖尿病中,单细胞活性和LDL的改变尚不清楚.
- 研究RRR-alpha-tocopherol (AT) 对这些因素的影响至关重要.
研究的目的:
- 为了比较2型糖尿病患者 (DM2-MV) 和没有 (DM2) 大血管疾病的LDL修饰,单细胞亲动质性活性和可溶性细胞粘附分子 (sCAM),与对照.
- 评估RRR-alpha-tocopherol (AT) 治疗对三组这些参数的影响.
主要方法:
- 对LDL糖化和氧化进行比较分析.
- 对单细胞超氧化离子 (O(2)(-)) 和互白素-1β (IL-1β) 的释放进行评估.
- 测量单细胞对内皮的粘附和循环中的sCAMs水平.
- 干预RRR-α-托科菲罗尔 (AT) 剂量为1200 IU/天,持续3个月.
主要成果:
- 在糖尿病组中,LDL糖化增加了,AT治疗没有影响.
- 在所有组中,AT疗法降低了LDL的氧化能力.
- 与对照人群相比,糖尿病单细胞显示增加了O(2)(-),IL-1β释放和内皮粘附.
- 在所有组中,AT疗法显著降低了单细胞O(2)(-),IL-1β,瘤缩因子-α和粘附.
- 在DM2和DM2-MV组之间没有发现单细胞活性或LDL参数的显著差异.
- 在糖尿病组中,sCAM水平升高,而在AT疗法下降.
结论:
- 2型糖尿病,不论巨大的血管并发症,增强单细胞的益动脉增生活性和粘附.
- RRR-alpha-tocopherol (AT) 疗法有效地减轻了这些与糖尿病相关的益风性变化.
- 这项研究为糖尿病中单细胞行为的新见解以及AT的治疗潜力提供了新的见解.
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