n-3 脂肪酸，而非 n-6 脂质体颗粒的摄取需要细胞表面锚定。
n-3, but not n-6 lipid particle uptake requires cell surface anchoring.
机构信息
Institute of Human Nutrition, College of Physicians and Surgeons, Columbia University, USA.
出版信息
Biochem Biophys Res Commun. 2010 Feb 5;392(2):135-9. doi: 10.1016/j.bbrc.2009.12.164. Epub 2010 Jan 7.
Omega-3 (n-3) fatty acids are emerging as bioactive agents protective against cardiovascular disease. However, their cellular delivery pathways are poorly defined. Here we questioned whether the uptake of n-3 triglyceride-rich particles (TGRP) is mediated by cell surface proteoglycans (PG) using LDL receptor (LDLR)+/+ and LDLR-/- cell models. LDLR+/+ but not LDLR-/- cells showed higher n-6 over n-3 TGRP uptake. Removal of cell surface proteins and receptors by pronase markedly enhanced the uptake of n-3 but not n-6 TGRP. Lactoferrin blockage of apoE-mediated pathways decreased the uptake of n-6 TGRP by up to 85% (p<0.05) but had insignificant effect on n-3 TGRP uptake. PG removal by sodium chlorate in LDLR+/+ cells substantially reduced n-3 TGRP uptake but had little effect on n-6 TGRP uptake. Thus, while n-6 TGRP uptake is preferentially mediated by LDLR-dependent pathways, the uptake of n-3 TGRP depends more on PG and non-LDLR cell surface anchoring.
ω-3（n-3）脂肪酸作为预防心血管疾病的生物活性物质而备受关注。然而，其细胞内的摄取途径尚不清楚。本研究旨在探讨富含 n-3 甘油三酯的颗粒（TGRP）是否通过细胞表面蛋白聚糖（PG）介导摄取，使用 LDL 受体（LDLR）+/+和 LDLR-/-细胞模型进行研究。结果显示，LDLR+/+细胞而非 LDLR-/-细胞对 n-6 与 n-3 TGRP 的摄取率更高。用链霉蛋白酶去除细胞表面蛋白和受体可显著增加 n-3 TGRP 的摄取，但对 n-6 TGRP 的摄取无明显影响。乳铁蛋白阻断 apoE 介导的途径可使 n-6 TGRP 的摄取减少 85%（p<0.05），但对 n-3 TGRP 的摄取影响不大。在 LDLR+/+细胞中用氯化钠去除 PG 可显著减少 n-3 TGRP 的摄取，但对 n-6 TGRP 的摄取影响较小。因此，尽管 n-6 TGRP 的摄取主要通过 LDLR 依赖途径介导，但 n-3 TGRP 的摄取更依赖于 PG 和非 LDLR 细胞表面锚定。
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