Flavonoids Identification and Pancreatic Beta-Cell Protective Effect of Lotus Seedpod

doi:10.3390/antiox9080658

中山醫學大學機構典藏 CSMUIR > 中山醫學大學研究成果 > 期刊論文 > Item 310902500/24370

Please use this identifier to cite or link to this item: https://ir.csmu.edu.tw:8080/ir/handle/310902500/24370

Title:	Flavonoids Identification and Pancreatic Beta-Cell Protective Effect of Lotus Seedpod
Authors:	Lee, MS;Chyau, CC;Wang, CP;Wang, TH;Chen, JH;Lin, HH
Keywords:	oxidative stress;pancreatic beta-cell;lotus seedpod;apoptosis;autophagy
Date:	2020
Issue Date:	2022-08-09T08:01:11Z (UTC)
Publisher:	MDPI
Abstract:	Oxidative stress is highly associated with the development of diabetes mellitus (DM), especially pancreatic beta-cell injury. Flavonoids derived from plants have caused important attention in the prevention or treatment of DM. Lotus seedpod belongs to a traditional Chinese herbal medicine and has been indicated to possess antioxidant, anti-age, anti-glycative, and hepatoprotective activities. The purpose of this study was to demonstrate the pancreatic beta-cell protective effects of lotus seedpod aqueous extracts (LSE) against oxidative injury. According to HPLC/ESI-MS-MS method, LSE was confirmed to have flavonoids derivatives, especially quercetin-3-glucuronide (Q3G). In vitro, LSE dose-dependently improved the survival and function of rat pancreatic beta-cells (RIN-m5F) from hydrogen peroxide (H2O2)-mediated loss of cell viability, impairment of insulin secretion, and promotion of oxidative stress. LSE showed potential in decreasing the H2O2-induced occurrence of apoptosis. In addition, H2O2-triggered acidic vesicular organelle formation and microtubule-associated protein light chain 3 (LC3)-II upregulation, markers of autophagy, were increased by LSE. Molecular data explored that antiapoptotic and autophagic effects of LSE, comparable to that of Q3G, might receptively be mediated via phospho-Bcl-2-associated death promoter (p-Bad)/B-cell lymphoma 2 (Bcl-2) and class III phosphatidylinositol-3 kinase (PI3K)/LC3-II signal pathway. In vivo, LSE improved the DM symptoms and pancreatic cell injury better than metformin, a drug that is routinely prescribed to treat DM. These data implied that LSE induces the autophagic signaling, leading to protect beta-cells from oxidative stress-related apoptosis and injury.
URI:	http://dx.doi.org/10.3390/antiox9080658 https://www.webofscience.com/wos/woscc/full-record/WOS:000564877300001 https://ir.csmu.edu.tw:8080/handle/310902500/24370
Relation:	ANTIOXIDANTS ,2020 ,v9 ,issue 8
Appears in Collections:	[中山醫學大學研究成果] 期刊論文

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