Flavonoids from Camellia sinensis (L.) O. Kuntze seed ameliorates TNF-a induced insulin resistance in HepG2 cells

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题名:	Flavonoids from Camellia sinensis (L.) O. Kuntze seed ameliorates TNF-a induced insulin resistance in HepG2 cells
作者:	Chen, Fu-Chih;Shen, Kuo-Ping;Ke, Liang-Yin;Lin, Hui-Li;Wu, Chia-Chang;Shaw, Shyh-Yu
关键词:	Flavonoids;Camellia sinensis (L.) O. Kuntze seed;TNF-a;Insulin resistance
日期:	2019-06-28
上传时间:	2019-07-03T02:23:57Z (UTC)
摘要:	The aim of this study is to discuss the non-catechin flavonoids (NCF) from Camellia sinensis (L.) O. Kuntze seed improving TNF-a impaired insulin stimulated glucose uptake and insulin signaling. Flavonoids had anti-metabolic syndrome and anti-inflammatory properties. It had widely been known for biological activity of catechins in tea, but very few research reports discussed the biological activity of noncatechin flavonoids in tea seed. We used HepG2 cell to treat with 5 lM insulin or with 5 lM insulin + 30 ng/ml TNF-a. Detecting the glucose concentration of medium, insulin decreased the glucose levels of medium meant that insulin promoted glucose uptake into cells, but TNF-a inhibited the glucose uptake effect of insulin. Furthermore, insulin increased the protein expressions of IR, IRS-1, IRS-2, PI3K-a, Akt/ PKB, GLUT-2, AMPK, GCK, pyruvate kinase, and PPAR-c. TNF-a activated p65 and MAPKs (p38, JNK1/2 and ERK1/2), iNOS and COX-2 which worsened the insulin signaling expressions of IR, IRS-1, IRS-2, PI3K-a, Akt/PKB, GLUT-2, AMPK, GCK, pyruvate kinase, and PPAR-c. We added NCF (500, 1000, 2000 ppm) to cell with insulin and TNF-a. Not only glucose levels of medium were lowered, and the protein expressions of insulin signaling were increased, but p38, JNK1/2, iNOS and COX-2 were also reduced. NCF could ameliorate TNF-a induced insulin resistance through inhibiting p38, JNK1/2, iNOS and COX-2, and suggested that it might be used in the future to help control insulin resistance. This finding is the first report to present the discovery. _ 2019 The Authors. Production and hosting by Elsevier B.V. on behalf of King Saud University. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
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