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Abstract

Effect of Chinese Herbal Decanoylacetaldehyde on Non-Alcoholic Fatty Liver Disease and its Mechanism

Author(s): Rong Zou and Yan Zhang*
Department of Gastroenterology, Wuhan University of Science and Technology Affiliated Puren Hospital, Wuhan, Hubei 430081, China

Correspondence Address:
Yan Zhang, Department of Gastroenterology, Wuhan University of Science and Technology Affiliated Puren Hospital, Wuhan, Hubei 430081, China, E-mail: yank1223@163.com


Non-alcoholic fatty liver disease is a common clinical chronic liver disease. It is a risk factor leading to liver cirrhosis, hepatocellular carcinoma and cardiovascular diseases. Decanoylacetaldehyde is the main medicinal component of Yuxingcao (Houttuynia cordata), which has specific effects in inflammatory diseases. BRL-3A cells were induced into non-alcoholic fatty liver disease cell model using oleic acid and palmitic acid. Different concentrations of decanoylacetaldehyde and p38 mitogen-activated protein kinase activator (metformin water) were used to intervene in the non-alcoholic fatty liver disease cell model. 250 μm oleic acid and 250 μm palmitic acid significantly reduced triglyceride content in cells without inhibiting the proliferation of non-alcoholic fatty liver disease cells. As the concentration of decanoylacetaldehyde intervention increased, the apoptosis rate of non-alcoholic fatty liver disease cells, the messenger ribonucleic acid level of interleukin-6, the protein levels of peroxisome proliferatoractivated receptor gamma, sterol regulatory element binding proteins-1c, p-p38mitogen-activated protein kinase and p-Jun N-terminal kinase were significantly decreased, and the cell survival rate, the messenger ribonucleic acid level of interleukin-10 and the protein level of peroxisome proliferatoractivated receptor alpha were significantly increased. Compared with the control group, there was a significant increase in the area of oil red O staining, triglyceride content, and sterol regulatory element binding proteins-1c protein levels, and a significant decrease in the protein level of peroxisome proliferator-activated receptor alpha in the model group. Compared with the model group, the area of oil red O staining, triglyceride content, peroxisome proliferator-activated receptor gamma and sterol regulatory element binding proteins-1c protein levels were significantly reduced and the protein level of peroxisome proliferator-activated receptor alpha was significantly increased in the decanoylacetaldehyde group. Compared with the metformin water group, the area of oil red O staining, total cholesterol content, peroxisome proliferator-activated receptor gamma and sterol regulatory element binding proteins-1c protein levels were significantly reduced and the protein level of peroxisome proliferatoractivated receptor alpha was significantly increased in the decanoylacetaldehyde+metformin water group. Decanoylacetaldehyde reduces adipocyte differentiation and inflammatory factor expression and alleviates non-alcoholic fatty liver disease progression by inhibiting p38 mitogen-activated protein kinase and p-Jun N-terminal pathway activation in non-alcoholic fatty liver disease cells.

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