Postprandial hypertriglyceridemia is an independent risk factor for cardiovascular disease. The aim of this study was to assess the effects of a single fat-rich meal on barrier functions and inflammatory status on human umbilical vascular endothelial cells (HUVECs), furthermore we assess the effects of mixture of palmitic acid and 25-hydroxycholesterol (PA +25OHCH) on integrity of endothelial cells and their inflammatory properties. HUVECs were induced with serum of healthy volunteers taken before, and 3 h after, the consumption of a meal with a standardized daily required dose of fats. In addition, endothelial cells were induced with PA +25OHCH (800 μM/L+10 μg/mL). Total cholesterol, triglycerides (TGs), high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, high sensitivity c-reactive protein, and glucose were measured at fasting and postprandially. HUVEC integrity was measured in the RTCA-DP xCELLigence system. mRNA expression of interleukin (IL)-33, IL-32, intercellular adhesion molecule-1 (ICAM-1), monocyte chemoattractant protein-1 (MCP-1), CX3C-chemokine, vascular endothelial growth factor (VEGF) occludin, and VE-cadherin was analyzed by real-time polymerase chain reaction. Viability and apoptosis were assessed in flow cytometry. The level of VEGF and IL-33 in fasting and postprandial serum was assessed by enzyme-linked immunosorbent assay (ELISA). Three hours after consumption of a fatty meal, all patients displayed increased levels of TGs and Toll-like receptors (110 ± 37 mg/dL versus 182 ± 64 mg/dL P < 0.05) (24 ± 11 mg/dL versus 42 ± 14 mg/dL P < 0.05). Postprandial serum and PA +25OHCH caused >20% decrease of HUVEC integrity than fasting serum (P < 0.001). HUVEC disintegration was accompanied by a decrease of occludin mRNA expression as compared with fasting serum (P < 0.05). The fatty meal affected neither VE-cadherin mRNA expression nor its apoptosis (P > 0.05). Mixture of PA +25OHCH caused decrease of VE-cadherin mRNA expression as compared with fasting serum (P < 0.01). PA +25OHCH did not affect HUVEC apoptosis (P > 0.05). Postprandial serum and PA +25OHCH caused increase of IL-33, MCP-1, ICAM-1, IL-32, VEGF, and CX3C-chemokine mRNA expression as compared with fasting serum (P < 0.05). Moreover, level of VEGF in fatty serum was significantly higher (P < 0.001). Postprandial lipemia after a single fatty meal may destabilize the endothelial barrier and initiate inflammatory processes.

中文翻译：

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单一的富含甘油三酯的膳食会破坏屏障功能并引发内皮细胞的炎症过程。

餐后高甘油三酯血症是心血管疾病的独立危险因素。本研究的目的是评估单一富含脂肪的膳食对人脐带血管内皮细胞 (HUVEC) 的屏障功能和炎症状态的影响，此外我们还评估了棕榈酸和 25-羟基胆固醇 (PA + 25OHCH) 对内皮细胞完整性及其炎症特性的影响。HUVECs 是用健康志愿者的血清诱导的，在食用具有标准化每日所需脂肪剂量的膳食之前和之后 3 小时。此外，用 PA +25OHCH (800 μM/L+10 μg/mL) 诱导内皮细胞。总胆固醇、甘油三酯 (TG)、高密度脂蛋白胆固醇、低密度脂蛋白胆固醇、高敏 c 反应蛋白、空腹和餐后测量血糖。HUVEC 完整性在 RTCA-DP xCELLigence 系统中测量。白细胞介素 (IL)-33、IL-32、细胞间粘附分子-1 (ICAM-1)、单核细胞趋化蛋白-1 (MCP-1)、CX3C-趋化因子、血管内皮生长因子 (VEGF) occludin 和VE-钙粘蛋白通过实时聚合酶链反应进行分析。在流式细胞术中评估活力和细胞凋亡。通过酶联免疫吸附测定（ELISA）评估空腹和餐后血清中VEGF和IL-33的水平。食用脂肪餐后三小时，所有患者都显示出 TG 和 Toll 样受体水平升高（110 ± 37 mg/dL vs 182 ± 64 mg/dL P < 0.05）（24 ± 11 mg/dL vs 42 ± 14毫克/分升 P < 0.05)。餐后血清和PA+25OHCH引起> HUVEC 完整性比空腹血清降低 20%（P < 0.001）。与空腹血清相比，HUVEC 解体伴随 occludin mRNA 表达的降低（P < 0.05）。脂肪餐既不影响 VE-钙粘蛋白 mRNA 表达，也不影响其细胞凋亡（P > 0.05）。与空腹血清相比，PA +25OHCH 的混合物导致 VE-钙粘蛋白 mRNA 表达降低（P < 0.01）。PA +25OHCH 不影响 HUVEC 凋亡（P > 0.05）。与空腹血清相比，餐后血清和PA+25OHCH导致IL-33、MCP-1、ICAM-1、IL-32、VEGF和CX3C-趋化因子mRNA表达增加（P < 0.05）。此外，脂肪血清中的VEGF水平显着升高（P < 0.001）。单次高脂肪餐后的餐后脂血症可能会破坏内皮屏障并引发炎症过程。