Hui Zhang1, Yi-Yang Hu, Qin Feng. 1. Shuguang Hospital Affiliated to Shanghai University of TCM, Institute of Liver Disease of Shanghai University of TCM, Shanghai.
Abstract
OBJECTIVE: To study the effects of Qushi Huayu Decoction (QHD) contained serum on fatty deposition and tumor necrosis factor alpha (TNF-alpha) secretion of hepatic lipotoxicity model in vitro, for further investigating the mechanism of the decoction for preventing and treating fatty liver. METHODS: The steatosis with TNF-alpha secretion lipotoxic model of HepG2 induced by long-chain free fatty acid (FFA) was duplicated. Groups of normal, model cells and model cells treated with different concentrations of QHD contained serum were set up to test the content of TNF-alpha in culture supernate and triglyceride (TG) in cells, as well as to observe the ultrastructural change of cells by oil-red staining and the protein expression and gene expression of cellular TNF-alpha. RESULTS: After being stimulated with FFA for 24 h, marked deposition of lipid with high content of TG presented in the cells of model group. Compared with the normal group, not only TNF-alpha content of culture supernate but also the protein expression and mRNA expression of intracellular TNF-alpha increased significantly. Contrast to the model group, the contents of TG in cells and TNF-alpha in supernate as well as the protein and mRNA expression of TNF-alpha in the model cell group treated with 10% QHD were lower significantly (all P < 0.01). CONCLUSION: QHD could significantly inhibit the fatty deposition and TNF-alpha secretion in HepG2 cells induced by free fatty acid.
OBJECTIVE: To study the effects of Qushi Huayu Decoction (QHD) contained serum on fatty deposition and tumor necrosis factor alpha (TNF-alpha) secretion of hepatic lipotoxicity model in vitro, for further investigating the mechanism of the decoction for preventing and treating fatty liver. METHODS: The steatosis with TNF-alpha secretion lipotoxic model of HepG2 induced by long-chain free fatty acid (FFA) was duplicated. Groups of normal, model cells and model cells treated with different concentrations of QHD contained serum were set up to test the content of TNF-alpha in culture supernate and triglyceride (TG) in cells, as well as to observe the ultrastructural change of cells by oil-red staining and the protein expression and gene expression of cellular TNF-alpha. RESULTS: After being stimulated with FFA for 24 h, marked deposition of lipid with high content of TG presented in the cells of model group. Compared with the normal group, not only TNF-alpha content of culture supernate but also the protein expression and mRNA expression of intracellular TNF-alpha increased significantly. Contrast to the model group, the contents of TG in cells and TNF-alpha in supernate as well as the protein and mRNA expression of TNF-alpha in the model cell group treated with 10% QHD were lower significantly (all P < 0.01). CONCLUSION: QHD could significantly inhibit the fatty deposition and TNF-alpha secretion in HepG2 cells induced by free fatty acid.