详细信息

Caffeic Acid Phenethyl Ester (Propolis Extract) Ameliorates Insulin Resistance by Inhibiting JNK and NF-κB Inflammatory Pathways in Diabetic Mice and HepG2 Cell Models  ( SCI-EXPANDED收录 EI收录)  

文献类型:期刊文献

英文题名:Caffeic Acid Phenethyl Ester (Propolis Extract) Ameliorates Insulin Resistance by Inhibiting JNK and NF-κB Inflammatory Pathways in Diabetic Mice and HepG2 Cell Models

作者:Nie, Jiarui[1];Chang, Yaning[1];Li, Yujia[1];Zhou, Yingjun[1];Qin, Jiawen[1];Sun, Zhen[1];Li, Haibin[2]

机构:[1]East China Univ Sci & Technol, Coll Bioengn, State Key Lab Bioreactor Engn, Shanghai 200237, Peoples R China;[2]Bee Forest Ind Co LTD, Shanghai 200030, Peoples R China

年份:2017

卷号:65

期号:41

起止页码:9041

外文期刊名:JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY

收录:;EI(收录号:20174304288096);WOS:【SCI-EXPANDED(收录号:WOS:000413503000009)】;

基金:This research work was supported by China Spark Program of Shanghai Municipal Agricultural Commission [Grant (2014)-6-1-2].

语种:英文

外文关键词:caffeic acid phenethyl ester; insulin resistance; inflammation; JNK; NF-kappa B

摘要:Caffeic acid phenethyl ester (CAPE), extracted from propolis, was evaluated for the ameliorative effects on insulin resistance and the mechanisms were identified, using non-insulin-dependent diabetes mellitus (NIDDM) model mice and insulin resistance (IR) model cells. After 5 weeks of CAPE supplementation, insulin sensitivity, hyperlipidemia, and peroxisome proliferator-activated receptor-alpha (PPAR-alpha) levels were improved in mice. Proinflammatory cytokines in serum and the expressions of tumor necrosis factor-alpha (TNF-alpha) mRNA in tissues were markedly downregulated from CAPE-treated mice. In vitro, CAPE supplement significantly improved glucose consumption, glucose uptake, glycogen content, and oxidative stress and decreased expression of glucose-6-phosphatase (G6Pase) mRNA in cells. Both in vivo and in vitro, CAPE enhanced p-Akt (Ser473) and p-insulin receptor substrate (IRS)-1 (Tyr612), but inhibited p-JNK (Thr183/Tyr185), p-NF-kappa B p65 (Ser536), and nuclear translocation of p-NF-kappa B p65 (Ser536). In summary, CAPE can ameliorate insulin resistance through modulation of JNK and NF-kappa B signaling pathway in mice and HepG2 cells.

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