番石榴葉萃取物抑制低密度脂蛋白氧化與保護氧化型低密度脂蛋白所誘發內皮細胞損傷之研究

Inhibitory Effects of Psidium guajava extract on Low-Density Lipoprotein (LDL) Oxidation and Oxidized LDL-Induced Cytotoxicity in Endothelial Cells

郭小萍(Hsiao-Ping Kuo)

指導教授 ： 朱淑珍

中臺科技大學/健康科學院/食品科技研究所/碩士(2011年)

摘要

心臟疾病以及腦血管疾病是國人十大死因中排名第二名和第三名。而動脈粥樣硬化是由於脂質的沉積而引發的慢性炎症的反應，並會造成內皮的損傷，及動脈壁纖維化。在粥狀動脈硬化的形成中氧化型低密度脂蛋白（oxidative modification of low-density lipoprotein;ox-LDL）扮演著重要的角色。在亞洲，中草藥被用來當作一種民間醫藥已有很長的一段時間；其中有許多中草藥已被發現具有廣泛的藥理和生化作用。近來也有文獻指出，番石榴是具有抗氧化，抗發炎和抗癌的生物活性。但番石榴葉對於保護作低密度脂蛋白的氧化和血管內皮的損傷及其詳細的作用機制到目前為止還不清楚。我們首次證實番石榴葉具有抑制LDL的氧化作用並且保護氧化型低密度脂蛋白對人類血管內皮細胞(HUVEC) 所造成的傷害。針對抑制LDL氧化實驗中，利用relative electrophoretic mobility (REM) shift assays、electrophoresis of ApoB fragmentation、lipid peroxidation assay，diene conjugation assay，和DPPH radical scavenging assay.證實番石榴葉可有效抑制硫酸銅所誘導LDL的氧化。在氧化型低密度脂蛋白對人類血管內皮細胞所造成的傷害實驗中，番石榴葉同時也可抑制氧化型低密度脂蛋白誘發人類臍靜脈內皮細胞的損傷，主要是透過抑制氧化型低密度脂蛋白所破壞粒腺體膜電位(mitochondrial membrane potential) 及抑制細胞凋亡過程中所釋放出的Bax並使得 pro-apoptosis protein Bcl-2之活化，此外，番石榴葉同時也可降低氧化型低密度脂蛋白誘發人類內皮細胞的細胞內導致ROS的產生。綜合以上結果，番石榴葉或許可應用於臨床上保護氧化型低密度脂蛋白所造成內皮細胞的功能失調及傷害。

關鍵字

番石榴 ； 內皮細胞損傷

並列摘要

Heart and cerebrovascular diseases are the second and third causes of death in Taiwan. Atherogenesis is characterized by lipid deposition, a chronic inflammatory response, endothelial injury, and chronic wound healing processes. The oxidative modification of low-density lipoprotein (LDL) is thought to have a central role in the pathogenesis of atherogenesis. Chinese herbs have been used as a folk medicine in Asia for a long time. Many of them have been found to exhibit a wide range of pharmacological and biochemical effects. Psidium guajava L. was a popular folk medicine and has several proven biological activities including antioxidant, anti-inflammatory and anticancer biological. However, its protective effects on LDL oxidation and endothelial injury induced by oxidized LDL (oxLDL) remain unclear. In this study, we evaluated the antioxidative activity of Psidium guajava L. extracts (PGE) and how PGE rescues human umbilical vein endothelial cells (HUVECs) from oxLDL-mediated dysfunction. The antioxidative activity of PGE was defined by the relative electrophoretic mobility of oxLDL, fragmentation of ApoB, diene conjugation assay, and the DPPH radical scavenging assay. PGE also inhibited the generation of ROS and the subsequent mitochondrial membrane potential collapse in HUVEC. Our results suggest that PGE may protect LDL oxidation and prevent oxLDL-induced cellular dysfunction.

並列關鍵字

Psidium guajava extract ； Induced Cytotoxicity in Endothelial Cells

參考文獻

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