Aqueous Mulberry Leaf Extract Ameliorates Alcoholic Liver Injury Associating with Upregulation of Ethanol Metabolism and Suppression of Hepatic Lipogenesis

Yi-Ju Lee; Ming-Chang Tsai; Hui-Ting Lin; Chau-Jong Wang; Shao-Hsuan Kao

doi:10.1155/2021/6658422

Aqueous Mulberry Leaf Extract Ameliorates Alcoholic Liver Injury Associating with Upregulation of Ethanol Metabolism and Suppression of Hepatic Lipogenesis

Evid Based Complement Alternat Med. 2021 May 8:2021:6658422. doi: 10.1155/2021/6658422. eCollection 2021.

Authors

Yi-Ju Lee^{1

2}, Ming-Chang Tsai^{3

4}, Hui-Ting Lin⁵, Chau-Jong Wang^{5

6

7}, Shao-Hsuan Kao^{5

6}

Affiliations

¹ Department of Pathology, Chung Shan Medical University Hospital, Taichung 402, Taiwan.
² Department of Pathology, School of Medicine, Chung Shan Medical University, Taichung 402, Taiwan.
³ School of Medicine, Chung Shan Medical University, Taichung 402, Taiwan.
⁴ Division of Gastroenterology and Hepatology, Department of Internal Medicine, Chung Shan Medical University Hospital, Taichung 402, Taiwan.
⁵ Institute of Medicine, Chung Shan Medical University, Taichung 402, Taiwan.
⁶ Clinical Laboratory, Chung Shan Medical University Hospital, Taichung 402, Taiwan.
⁷ Department of Health Diet and Industry Management, Chung Shan Medical University, Taichung 402, Taiwan.

Abstract

Excessive alcohol intake is a major cause of chronic liver damage and is highly associated with the development of a spectrum of hepatic disorders, including steatohepatitis, liver cirrhosis, and liver cancer. Thus, we aimed to explore the hepatoprotective effects of an aqueous mulberry leaf extract (AME) on alcoholic fatty liver disorder (AFLD) by using a mouse model fed with excessive ethanol. Compared with the normal diet, the ethanol diet significantly increased the body weight of the mice, while the AME supplement reduced the weight gain caused by the ethanol diet. The ethanol diet also attenuated the activity of alcohol dehydrogenase and antioxidant enzymes but increased lipid peroxidation in the liver, which were reversed by AME supplementation. Additionally, AME supplementation diminished the ethanol diet-induced hepatic leukocyte infiltration and expressions of IL-6 and TNFα. Moreover, AME supplementation also reduced the ethanol-diet-induced lipid accumulation and expression of 1-acylglycerol-3-phosphate acyltransferase, acetyl-CoA carboxylase, low-density lipoprotein receptor, and sterol regulatory element-binding protein-1/2 in the liver. Collectively, AME supplementation improved liver lipid accumulation and proinflammatory response in mice induced by the ethanol diet, which was associated with the upregulation of ethanol-metabolizing enzymes and the downregulation of lipogenesis components.