Abstract

Honey-processed Astragalus (HPA) is a mixture of Astragalus and honey, which is a processed product of Chinese medicine. It has the active ingredients of Astragalus and the unique effects of honey. However, the mechanism of HPA for improving alcoholic liver disease (ALD) is not clear. The purpose of this study is to explore the ameliorating effect and mechanism of HPA (4 and 8 g/kg bw) on alcoholic liver injury. Two doses of HPA were orally administered to alcohol-treated mice for four weeks. The results showed that HPA could effectively reduce triglycerides (TG) by 59% and free fat acid (FFA) and total cholesterol (TC) in serum and hepatic were reduced by least 25.9%. HPA could cause a decrease in serum low-density lipoprotein cholesterol (LDL-C) from 0.145 mM to 0.117 mM, and the serum high-density lipoprotein cholesterol (HDL-C) was increased. After alcohol-treated mice were supplemented with HPA, antioxidant markers (superoxide dismutase (SOD), catalase (CAT), glutathione (GSH), and Glutathione peroxidase (GSH-Px)), liver function index (alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP)), proinflammatory cytokines (tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-1β (IL-1β)), and liver tissue were all significantly improved. This is related to the fact that HPA can promote the expression of oxidative stress-related genes and inhibit the expression of inflammation-related genes. In addition, HPA could also regulate the disturbance of the intestinal microflora. In general, HPA could significantly improve the accumulation of serum and liver lipids caused by alcohol and the imbalance of intestinal flora in mice. It could also improve liver function, oxidative stress, and inflammation.

Highlights

  • Alcohol-related diseases are one of the most common preventable diseases in the world [1]

  • In view of the above biological activities of Honey-processed Astragalus (HPA), we speculate that HPA may have a beneficial effect on improving alcoholic liver disease (ALD). erefore, this study aims to evaluate the improvement effect of HPA (Hunyuan, Shanxi Province) on alcohol-induced liver injury in mice and the effect of reducing serum and hepatic lipids

  • Edible alcohol was purchased from Henan Xinheyang Alcohol Co., Ltd. (Henan, China). e assay kits of CAT, superoxide dismutase (SOD), GSH, MDA, c-glutamyl transpeptidase (c-GT), glutathione peroxidase (GSH-Px), and free fat acid (FFA) and the commercial enzyme-linked immunosorbent assay (ELISA) kits of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-1β (IL-1β) were bought from Beijing Sinouk Institute of Biological Technology (Beijing, China). e commercial assay kits of TG, total cholesterol (TC), highdensity lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP) were purchased from Biosino Bio-Technology and Science Inc. (Beijing, China)

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Summary

Introduction

Alcohol-related diseases are one of the most common preventable diseases in the world [1]. Alcohol injury can cause damage to many end-organs and systems in the body, and alcoholic liver disease (ALD) is an important manifestation of liver injury [3]. Ere is evidence that the development mechanism of ALD is closely related to oxidative stress, inflammatory development, and intestinal microflora disorders [5]. ALD can develop from asymptomatic to alcoholic fatty liver, liver cirrhosis, and even alcoholic hepatitis and hepatocellular carcinoma [2, 4]. Drugs such as disulfiram, naltrexone, and corticosteroids are used in abstinence treatment, some drugs are not approved for ALD treatment. Due to the personal differences of patients and adverse reactions

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