TY - JOUR
T1 - Flavonoids from Camellia sinensis (L.)O. Kuntze seed ameliorates TNF-α induced insulin resistance in HepG2 cells
AU - Chen, Fu Chih
AU - Shen, Kuo Ping
AU - Ke, Liang Yin
AU - Lin, Hui Li
AU - Wu, Chia Chang
AU - Shaw, Shyh Yu
N1 - Funding Information:
This work was supported by grants 105-FI-DON-IAC-R-002 and 106-FI-DBS-IAC-R-001 to Dr. Kuo-Ping Shen from Pingtung Christian Hospital, Pingtung, Taiwan, and MOST 105-2320-B-276-003-MY2 to Dr. Hui-Li Lin from Ministry of Science and Technology, Taiwan. We would like to thank Miss Tsui-Jung Lin for her technical advice and support.
Funding Information:
This work was supported by grants 105-FI-DON-IAC-R-002 and 106-FI-DBS-IAC-R-001 to Dr. Kuo-Ping Shen from Pingtung Christian Hospital, Pingtung, Taiwan , and MOST 105-2320-B-276-003-MY2 to Dr. Hui-Li Lin from Ministry of Science and Technology, Taiwan. We would like to thank Miss Tsui-Jung Lin for her technical advice and support.
Publisher Copyright:
© 2019 The Authors
PY - 2019/5
Y1 - 2019/5
N2 - The aim of this study is to discuss the non-catechin flavonoids (NCF)from Camellia sinensis (L.)O. Kuntze seed improving TNF-α 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 non-catechin flavonoids in tea seed. We used HepG2 cell to treat with 5 μM insulin or with 5 μM insulin + 30 ng/ml TNF-α. Detecting the glucose concentration of medium, insulin decreased the glucose levels of medium meant that insulin promoted glucose uptake into cells, but TNF-α inhibited the glucose uptake effect of insulin. Furthermore, insulin increased the protein expressions of IR, IRS-1, IRS-2, PI3K-α, Akt/PKB, GLUT-2, AMPK, GCK, pyruvate kinase, and PPAR-γ. TNF-α 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-α, Akt/PKB, GLUT-2, AMPK, GCK, pyruvate kinase, and PPAR-γ. We added NCF (500, 1000, 2000 ppm)to cell with insulin and TNF-α. 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-α 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.
AB - The aim of this study is to discuss the non-catechin flavonoids (NCF)from Camellia sinensis (L.)O. Kuntze seed improving TNF-α 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 non-catechin flavonoids in tea seed. We used HepG2 cell to treat with 5 μM insulin or with 5 μM insulin + 30 ng/ml TNF-α. Detecting the glucose concentration of medium, insulin decreased the glucose levels of medium meant that insulin promoted glucose uptake into cells, but TNF-α inhibited the glucose uptake effect of insulin. Furthermore, insulin increased the protein expressions of IR, IRS-1, IRS-2, PI3K-α, Akt/PKB, GLUT-2, AMPK, GCK, pyruvate kinase, and PPAR-γ. TNF-α 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-α, Akt/PKB, GLUT-2, AMPK, GCK, pyruvate kinase, and PPAR-γ. We added NCF (500, 1000, 2000 ppm)to cell with insulin and TNF-α. 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-α 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.
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U2 - 10.1016/j.jsps.2019.01.014
DO - 10.1016/j.jsps.2019.01.014
M3 - Article
AN - SCOPUS:85060913685
VL - 27
SP - 507
EP - 516
JO - Saudi Pharmaceutical Journal
JF - Saudi Pharmaceutical Journal
SN - 1319-0164
IS - 4
ER -