Journal
AMERICAN JOURNAL OF CHINESE MEDICINE
Volume 44, Issue 4, Pages 755-769Publisher
WORLD SCIENTIFIC PUBL CO PTE LTD
DOI: 10.1142/S0192415X16500415
Keywords
Timosaponin B-II; Insulin Resistance; Inflammation; IR/IRS-1/PI3K/Akt; IKK/NF-kappa B
Funding
- National Natural Science Foundation of China [81403080, 81303223]
- Natural Science Foundation of Jiangsu Province [BK20140674]
- Fundamental Research Funds for the Central Universities
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This study aimed to investigate the effect of timosaponin B-II (TB-II) on palmitate (PA)-induced insulin resistance and inflammation in HepG2 cells, and probe the potential mechanisms. TB-II, a main ingredient of the traditional Chinese medicine Anemarrhena asphodeloides Bunge, notably ameliorated PA-induced insulin resistance and inflammation, and significantly improved cell viability, decreased PA-induced production of tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) levels. Further, TB-II treatment notably decreased malondialdehyde (MDA) and lactate dehydrogenase (LDH) levels, and improved superoxide dismutase (SOD) and nitric oxide (NO). TB-II also reduced HepG2 cells apoptosis. Insulin receptor substrate-1 (IRS1)/phosphatidylinositol 3-kinase (PI3K)/Akt and inhibitor of nuclear factor kappa-B kinase (IKK)/NF-kappa B pathways-related proteins, and IKK beta, p65 phosphorylation, serine phosphorylation of insulin receptor substrate-1 (IRS-1) at S307, tyrosine phosphorylation of IRS-1, and Akt activation were determined by Western blot. Compared to model group, TB-II significantly downregulated the expression of p-NF-kappa Bp65, p-IKK beta, p-IRS-1, p-PI3K and p-Akt. TB-II is a promising potential agent for the management of palmitate-induced insulin resistance and inflammation, which might be via IR/IRS-1/PI3K/Akt and IKK/NF-kappa B pathways.
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