Muscadine or amla extracts standardized to ellagic acid content ameliorate glucolipotoxicity associatedβ-cell dysfunction via inhibition of IL-1βand improved insulin secretion  

作　　者：Srikanth Earpina Karen McDonough Millicent Yeboah-Awudzi Kristina J.Cook Sita Aggarwal Jack N.Losso 

机构地区：[1]Chronic Degenerative Disease Prevention Laboratory,School of Nutrition and Food Science,Louisiana State University AgCenter,Louisiana State University System,Baton Rouge,LA 70803,USA [2]School of Animal Science,Louisiana State University AgCenter,Louisiana State University System,Baton Rouge,LA 70803,USA [3]William Hansel Cancer Prevention,Pennington Biomedical Research Center,Louisiana State University System,Baton Rouge,LA 70808,USA [4]Louisiana State University System,Baton Rouge,LA 70803,USA

出　　处：《Food Production, Processing and Nutrition》2020年第1期91-101,共11页食物生产加工与营养（英文）

摘　　要：Glucolipotocixity induces IL-1βsecretion which impairs pancreaticβ-cell insulin secretion.Ellagic acid and urolithin A have strong anti-inflammatory effect on cells.Muscadine and amla are very good sources of ellagic acid.The present study examined the effect of ellagic acid,ellagic acid-rich muscadine or amla extract,or urolothin A on inflammation inβcells under glucolipotoxic conditions.Rat NIT-1βcells were incubated in glucolipotoxic conditions(33.3 mM glucose,250μM palmitic acid or 33.3 mM glucose+250μM palmitic acid with or without ellagic acid,ellagic acid-rich muscadine or amla extracts standardized to its ellagic acid content,or urolithin A).Inflammatory status was evidenced by ELISA analysis of insulin and IL-1βsecretion.Ellagic acid-rich muscadine or amla extracts dose-dependently stimulated insulin secretion and down-regulated IL-1βbetter than pure ellagic acid,or urolithin A.Urolithin A did not statistically stimulate insulin secretion and did not inhibit IL-1β.

关 键 词：Muscadine Amla Ellagic acid NIT-1 pancreaticβ-cells glucose Palmitic acid GLUCOLIPOTOXICITY IL-1Β Inflammation INFLAMMASOME Insulin secretion 

分 类 号：R28[医药卫生—中药学]