Effects of Soothing Liver and Invigorating Spleen Recipe on Lipid Metabolism Disorders in Kupffer Cells of NAFLD Rats by LXRα/SREBP-1c Signal Pathway
10.1016/S1674-6384(14)60045-9
- Author:
Xiang-wen GONG
1
Author Information
1. Department of Traditional Chinese Medicine, The First Affiliated Hospital of Jinan University
- Publication Type:Journal Article
- Keywords:
Kupffer cells;
Lipid metabolism;
LXRα/SREBP-1c signaling pathway;
Non-alcoholic fatty liver disease;
Soothing liver and invigorating spleen recipe
- From:
Chinese Herbal Medicines
2014;6(4):297-304
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To investigate the mechanism of lipid metabolism disorders in Kupffer cells (KCs) of non-alcoholic fatty liver disease (NAFLD) rats mediated by LXRα-SREBP-1c pathway and the interference of soothing liver and invigorating spleen recipe (SLISR) on it. Methods: SD male rats were randomly divided into five groups: normal, model, soothing liver recipe (SLR), invigorating spleen recipe (ISR), and soothing liver and invigorating spleen recipe (SLISR) groups. The rats in treatment groups were administered for 8 weeks. The liver tissue was stained with H&E and oil red O. The levels of hepatic lipid and blood lipid were measured by biochemical analyzer. KCs were isolated from the livers of rats to evaluate the expression of LXRα, SREBP-1C, and FAS mRNA by real-time fluorescence quantitative PCR tests; LXRα, SREBP-1C, and FAS proteins were measured by Western blotting. Results: The H&E and oil red O staining results showed that the model rats successfully reproduced typical pathogenetic and histopathological features of NAFLD. The levels of hepatic lipid and blood lipid in the model rats were dramatically increased. Compared with the model group, the values of hepatic lipid and blood lipid in the treatment groups were significantly ameliorated (P < 0.05, 0.01). The yields of purified KCs from each rat were 2×107-3×107. The viability of KCs was higher than 95%, with the purity over 90.18%. Compared with the model group, the expression of LXRα, SREBP-1C, and FAS mRNA and proteins was decreased in all treatment groups, especially in the SLR group (P < 0.05). Conclusion: SLISR may protect liver against injury included by lipid metabolism disorders in KCs through LXRα/SREBP-1c signaling pathway, which may be an important mechanism for the prevention and treatment of NAFLD.
