Purple Sweet Potato Extracts Improve Oxidative Stress-induced Pancreatic β-cells Apoptosis

ASIA unversity > 醫學暨健康學院 > 食品營養與保健生技學系 > 博碩士論文 > Item 310904400/12544

Please use this identifier to cite or link to this item: http://asiair.asia.edu.tw/ir/handle/310904400/12544

Title:	Purple Sweet Potato Extracts Improve Oxidative Stress-induced Pancreatic β-cells Apoptosis
Authors:	Lee, Yi-Ying
Contributors:	Department of Health and Nutrition Biotechnology Lin, Chia-Yu
Keywords:	Pancreatic β-cells;purple sweet potato;oxidative stress
Date:	2012
Issue Date:	2012-11-18 08:30:04 (UTC+0)
Publisher:	Asia University
Abstract:	Pancreatic β-cells are relatively low in the expression of antioxidant enzymes, which render β-cells more susceptible to oxidative damage. It has been implied that purple sweet potatos (PSP) have anti-oxidative and anti-inflammatory effects, as well as may improve blood glucose levels, suggesting the potential benefits of PSP on diabetes. Therefore, the purpose of this study was to investigate the anti-apoptotic effects of PSP on pancreatic β-cells. INS-1 cells were treated with PSP and/or H2O2/STZ for variuos concentrations and time periods. Cell survival was detected by MTT, Sub G1 phase and western. The antioxidative effect of the PSP was determined by DPPH radical-scavenging activity, total phenolic determination, ferrous ion chelating activity, reducing power, Superoxide Dismutase (SOD) Activity, Glutathione Peroxidase (GPx) Activity, Catalase Activity and reactive oxygen species (ROS) assay. In addition, JC1 analysis and ATP assay, as well as insulin secretion were conducted to measure intracellular functions. Treatment of H2O2/STZ causes more than 50% of cell death, which is recovered by PSP treatment significantly. This improved cell survival by PSP could be due to the reduced caspase-3 expression. Moreover, PSP might act as an atioxidant, which inhibits more than 50% of the oxidative stress-induced intracellular ROS generation. Cellular ATP content and mitochondria membrane potential are also alleviated in the presence of PSP after oxidative stress. While insulin secretion after H2O2/STZ treatment is about one third of that of control, PSP dramatically recovers it. In summary, these findings indicate that PSP protects pancreatic β-cells from oxidative stress-induced apoptosis and improves insulin secretion. This enhanced cell survival could be partially due to the ability of PSP to scavenge free radical and maintain mitochondria function.
Appears in Collections:	[食品營養與保健生技學系] 博碩士論文

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