Liposomal Silybin Improves Glucose and Lipid Metabolisms in Type 2 Diabetes Mellitus Complicated with Non-Alcoholic Fatty Liver Disease via AMPK/TGF-<i>β</i>1/Smad Signaling

DOI Web Site PubMed 参考文献27件
  • Cai Jialuo
    School of Pharmacy, Hunan University of Chinese Medicine Preventive Treatment of Disease Center, The First Hospital of Hunan University of Chinese Medicine
  • Zhu Yilin
    Graduate School, Hunan University of Chinese Medicine
  • Li Xiaoping
    Preventive Treatment of Disease Center, The First Hospital of Hunan University of Chinese Medicine
  • Deng Guiming
    Scientific Research Section, The First Hospital of Hunan University of Chinese Medicine
  • Han Yuanshan
    Scientific Research Section, The First Hospital of Hunan University of Chinese Medicine
  • Yuan Feiyun
    Library, Hunan University of Chinese Medicine
  • Yi Gangqiang
    Party Committee, Hunan University of Chinese Medicine
  • Xia Xinhua
    School of Pharmacy, Hunan University of Chinese Medicine

抄録

<p>Improving hepatic glucose and lipid metabolisms is an important strategy to treat type 2 diabetes mellitus complicated with non-alcoholic fatty liver disease (T2DM-NAFLD). Silybin (SLB) has the potential hepatoprotection, while its oral bioavailability is poor. This study aims to investigate the functional role and mechanism of liposomal SLB in modulating glucose/lipid metabolism in T2DM-NAFLD. SLB was prepared by thin film dispersion method and characterized using dynamic light scattering, scanning electron microscope, high performance liquid chromatography and zeta potential analyzer. A rat model of T2DM-NAFLD was used to determine the role of liposomal SLB in regulating glycolipid metabolism and hepatic damage. Rat primary hepatocytes were used to demonstrate the hepatoprotection mechanism of liposomal SLB. The encapsulation efficiency was more than 80%, which showed the average particle size of 119.76 nm. Also, the average Zeta potential was −4.76 mV. These liposomes were spherical. In rats with T2DM-NAFLD, liposomal SLB alleviated insulin resistance and lipid metabolism, thereby improving hepatic lipid accumulation, inflammation and fibrosis. Besides, liposomal SLB elevated AMPK phosphorylation, and decreased collagen I/III, α-smooth muscle actin (α-SMA), transforming growth factor-β1 (TGF-β1) and the phosphorylation of Smad2/3. In hepatocyte model, compound C partially reversed the effects of liposomal SLB on cell viability, glycolipid metabolism and AMPK/TGF-β1/Smad pathway activation. Liposomal SLB ameliorates hepatic glucose and lipid metabolisms in T2DM-NAFLD via activating AMPK/TGF-β1/Smad pathway, providing an efficient strategy for treating T2DM-NAFLD.</p>

収録刊行物

参考文献 (27)*注記

もっと見る

キーワード

詳細情報 詳細情報について

問題の指摘

ページトップへ