期刊
EVIDENCE-BASED COMPLEMENTARY AND ALTERNATIVE MEDICINE
卷 2015, 期 -, 页码 -出版社
HINDAWI LTD
DOI: 10.1155/2015/643102
关键词
-
资金
- Natural Sciences Funds, China [81173626]
- Guangdong Province-Chinese Education Ministry Industry, Education and Research Cooperation Project [2011B090400379]
- Guangdong Province Natural Sciences Funds Research Team Project [10351022401000000]
The aim of our study is to elucidate the mechanisms of oleanolic acid (OA) on insulin resistance (IR) in HepG2 cells. HepG2 cells were induced with FFA as the insulin resistance model and were treated with OA. Then the glucose content and the levels of tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) were analyzed. Moreover, protein expression of nuclear factor kappa B (NF kappa B), insulin receptor substrate 1(IRS1), and glucose transporter 4 (GLUT4) in cells treated with OA were measured by Western blot analysis. Additionally, IRS1 protein expression exposed to OA was detected after using pyrrolidine dithiocarbamate (PDTC). Our results revealed that OA decreased the glucose content in HepG2 cells in vitro. Moreover, OA reduced the levels of TNF-alpha and IL-6 and upregulated IRS1 and GLUT4 protein expression. Furthermore, OA also reduced NF-kappa B protein expression in insulin-resistant HepG2 cells. After blocking NF-kappa B, the expression of IRS1 protein had no obvious changes when treated with OA. OA attenuated insulin resistance and decreased the levels of TNF-alpha and IL-6. Meanwhile, OA decreased NF-kappa B protein expression and upregulated IRS1 and GLUT4 protein expression. Therefore, regulating the IRS1-GLUT4 pathway via NF-kappa B was the underlying mechanism of OA on insulin resistance.
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