CAJ | 학술논문

目的探讨抗氧化剂对高密度脂蛋白(HDL)氧化修饰的抑制机制,为预防HDL的氧化修饰提供实验依据.方法将体外新鲜制备的人血浆HDL分别用不同浓度的硫酸铜(CuSO_4)、次氯酸(HOCl)处理或与动脉壁细胞共同温育进行氧化修饰,然后分别测定天然未修饰HDL(N-HDL)、氧化修饰HDL(Ox-HDL)的凝胶电泳相对电泳迁移率(REM)、硫代巴比妥酸反应物质(TBARS)、溶血卵磷脂/卵磷脂比率(LPC/PC)的生成及载脂蛋白成分改变.对比相同条件下,加入抗氧化剂叔丁基甲苯(BHT)、Vit E及Vit C后,以上指标的改变.结果 BHT、Vit E及Vit C均可显著抑制由Cu~(2+)和HOCl诱导的Ox-HDL的REM增加、TBARS的生成、卵磷脂的水解,载脂蛋白AⅠ和AⅡ的改变.动脉壁细胞诱导的Ox-HDL的琼脂糖REM增加、TRARS的生成及卵磷脂水解也可被BHT、Vit E及Vit C显著抑制.但不同抗氧化剂的作用方式各有不同.结论 BHT以及Vit E和Vit C能有效抑制体内外HDL的氧化修饰.
목적 탐토항양화제대고밀도지단백(HDL)양화수식적억제궤제,위예방HDL적양화수식제공실험의거.방법 장체외신선제비적인혈장HDL분별용불동농도적류산동(CuSO_4)、차록산(HOCl)처리혹여동맥벽세포공동온육진행양화수식,연후분별측정천연미수식HDL(N-HDL)、양화수식HDL(Ox-HDL)적응효전영상대전영천이솔(REM)、류대파비타산반응물질(TBARS)、용혈란린지/란린지비솔(LPC/PC)적생성급재지단백성분개변.대비상동조건하,가입항양화제숙정기갑분(BHT)、Vit E급Vit C후,이상지표적개변.결과 BHT、Vit E급Vit C균가현저억제유Cu~(2+)화HOCl유도적Ox-HDL적REM증가、TBARS적생성、란린지적수해,재지단백AⅠ화AⅡ적개변.동맥벽세포유도적Ox-HDL적경지당REM증가、TRARS적생성급란린지수해야가피BHT、Vit E급Vit C현저억제.단불동항양화제적작용방식각유불동.결론 BHT이급Vit E화Vit C능유효억제체내외HDL적양화수식.
Objective To study the role and mechanism of antioxidants on inhibiting oxidative modification of high density lipoproteins (HDL). Methods Freshly prepared human plasma HDL was treated by incubation with copper ion, hyperchlorite or arterial wall cells. Compared to control, the test groups were treated with addition of different concentration of butylhydroxytoluene (BHT), vitamin C and vitamin E. Then, the relative electrophoretic mobility (REM), thiobarbituric acid-reactive substances (TBARS), ratio of lysolecithin to lecithin (LPC/PC), and lipoprotein moieties were investigated. Results BHT, vitamin C and vitamin E can significantly inhibit the increasing REM, TBARS, LPC/PC ratio and lipoprotein variation that induced by copper ion and hyperchlorite and arterial wall cells. But these antioxidants act on different manner. Conclusion BHT, vitamin C and vitamin E can inhibit the oxidative modification of HDL and hence could be potential nutrients to prevent atherosclerosis.