Crude triterpenoid saponins from Ilex latifolia (Da Ye Dong Qing) ameliorate lipid accumulation by inhibiting SREBP expression via activation of AMPK in a non-alcoholic fatty liver disease model

摘要

Background Ilex latifolia Thunb. (Da Ye Dong Qing) is used for weight loss and for its antidiabetic effects. This study aims to investigate the beneficial effects and potential mechanisms of action of crude triterpenoid saponins (CTS) from I. latifolia in a mouse model of high-fat diet (HFD)-induced non-alcoholic fatty liver disease (NAFLD). Methods Male C57BL/6 mice (n?=?50), were arbitrarily divided into five groups (n?=?10 in each group): a control group, HFD group, simvastatin group (10?mg/kg/day), and two CTS treatment groups (100 and 200?mg/kg/day). All mice except those in the control group were fed an HFD for 4?weeks. Animals in the treatment groups were orally administered simvastatin or CTS for 8?weeks. Oral glucose tolerance tests and insulin tolerance tests were performed. At the end of treatment, plasma lipid levels, and oxidative parameters in the liver were measured using commercial test kits. Western blotting was used to evaluate whether CTS induced AMP-activated protein kinase (AMPK) and acetyl CoA carboxylase activation, and the expression of transcription factors and their target genes was evaluated in a quantitative PCR assay. Results Compared with the HFD group, the CTS (200?mg/kg/day) treatment group showed significantly decreased plasma lipid parameters (P?P?=?0.018, and P?=?0.005 for triglycerides, total cholesterol and low-density lipoprotein cholesterol, respectively), and improved insulin resistance (P?=?0.006). CTS (100 and 200?mg/kg/day) supplementation also reduced hepatic lipids and protected the liver from oxidative stress by attenuating malondialdehyde content (P?P?P?P?P?=?0.013, P?=?0.007, P?=?0.011, and P?=?0.014, respectively). Conclusion CTS from I. latifolia improved insulin resistance and liver injury in HFD-fed mice, and attenuated NAFLD via the activation of AMPK and inhibition of the gene expression of SREBPs and some of their target molecules.