Department of Food Science and Biotechnology, Division of Biotechnology, School of Bioscience and Biotechnology, Kangwon National University, Chuncheon, Korea.
Nutr Res. 2012 May;32(5):365-73. doi: 10.1016/j.nutres.2012.02.005. Epub 2012 Apr 19.
We hypothesized that a Platycodon grandiflorum root (PG) ethyl acetate extract (PGEA) would help reduce the vascular cell injury caused by oxidized low-density lipoprotein (oxLDL) and prevent high-fat (HF) diet-induced dyslipidemia and oxidative stress by up-regulating antioxidant proteins. We investigated the protective effects of PGEA against vascular endothelial cell injury induced by oxLDL and dyslipidemia induced by an HF diet, and the mechanisms underlying these effects were studied. The protective effects of PGEA were investigated with respect to calf pulmonary arterial endothelial (CPAE) cell viability and the lactate dehydrogenase release during oxLDL treatment. The in vivo effects of PGEA were examined using C57BL/6 mice, which were fed an HF diet for 9 weeks. The HF diet was supplemented with 0, 25, or 75 mg/kg PGEA during the last 4 weeks of the experimental period. Histologic analyses of hepatic lipid accumulation were performed. The changes in antioxidant protein levels induced by PGEA, which protects against HF diet-induced oxidative stress, were measured using a proteomics approach. We found that PGEA exhibited antioxidant activity. In CPAE cells, PGEA inhibited both oxLDL-induced cell death and lactate dehydrogenase release. In the HF diet-induced obese mice that received PGEA, we observed significantly reduced plasma and hepatic lipid levels, demonstrating that PGEA has beneficial effects on hyperlipidemia. In addition, we found that PGEA caused the up-regulation of antioxidant proteins. These findings suggest that the antioxidant effects of PGEA may protect against oxidative stress-related diseases.
我们假设，桔梗根乙酸乙酯提取物（PGEA）将有助于减少氧化型低密度脂蛋白（oxLDL）引起的血管细胞损伤，并通过上调抗氧化蛋白来预防高脂肪（HF）饮食引起的血脂异常和氧化应激。我们研究了 PGEA 对 oxLDL 诱导的血管内皮细胞损伤和 HF 饮食诱导的血脂异常的保护作用，并研究了这些作用的机制。通过小牛肺动脉内皮（CPAE）细胞活力和 oxLDL 处理期间乳酸脱氢酶释放来研究 PGEA 的保护作用。使用 C57BL/6 小鼠研究了 PGEA 的体内作用，这些小鼠在实验期间的最后 4 周内喂食 HF 饮食。对肝脏脂质积累的组织学分析进行了研究。使用蛋白质组学方法测量了 PGEA 对 HF 饮食诱导的氧化应激的保护作用所诱导的抗氧化蛋白水平的变化。我们发现 PGEA 具有抗氧化活性。在 CPAE 细胞中，PGEA 抑制 oxLDL 诱导的细胞死亡和乳酸脱氢酶释放。在接受 PGEA 的 HF 饮食诱导肥胖的小鼠中，我们观察到血浆和肝脏脂质水平明显降低，表明 PGEA 对高脂血症有有益的作用。此外，我们发现 PGEA 引起抗氧化蛋白的上调。这些发现表明，PGEA 的抗氧化作用可能有助于预防与氧化应激相关的疾病。
