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

碩士 === 中臺科技大學 === 食品科技研究所 === 99 === 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-...

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Bibliographic Details
Main Authors: Hsiao-Ping Kuo, 郭小萍
Other Authors: Shu-Chen Chu
Format: Others
Language:zh-TW
Published: 2011
Online Access:http://ndltd.ncl.edu.tw/handle/63998919693118171297
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Summary:碩士 === 中臺科技大學 === 食品科技研究所 === 99 === 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.