Abstract
Licochalcone A is a chalcone isolated from Glycyrrhiza uralensis. It showed anti-tumor and anti-inflammatory properties in mice with acute lung injuries and regulated lipid metabolism through the activation of AMP-activated protein kinase (AMPK) in hepatocytes. However, the effects of licochalcone A on reducing weight gain and improving nonalcoholic fatty liver disease (NAFLD) are unclear. Thus, the present study investigated whether licochalcone A ameliorated weight loss and lipid metabolism in the liver of high-fat diet (HFD)-induced obese mice. Male C57BL/6 mice were fed an HFD to induce obesity and NAFLD, and then were injected intraperitoneally with licochalcone A. In another experiment, a fatty liver cell model was established by incubating HepG2 hepatocytes with oleic acid and treating the cells with licochalcone A to evaluate lipid metabolism. Our results demonstrated that HFD-induced obese mice treated with licochalcone A had decreased body weight as well as inguinal and epididymal adipose tissue weights compared with HFD-treated mice. Licochalcone A also ameliorated hepatocyte steatosis and decreased liver tissue weight and lipid droplet accumulation in liver tissue. We also found that licochalcone A significantly regulated serum triglycerides, low-density lipoprotein, and free fatty acids, and decreased the fasting blood glucose value. Furthermore, in vivo and in vitro, licochalcone A significantly decreased expression of the transcription factor of lipogenesis and fatty acid synthase. Licochalcone A activated the sirt-1/AMPK pathway to reduce fatty acid chain synthesis and increased lipolysis and β-oxidation in hepatocytes. Licochalcone A can potentially ameliorate obesity and NAFLD in mice via activation of the sirt1/AMPK pathway.
Highlights
Obesity is becoming prevalent in developed and developing countries and is considered an important risk factor for chronic diseases including cardiovascular diseases, hypertension, osteoarthritis, some cancers, and diabetes [1]
Mice were weighed twice a week, and we found that the weight of high-fat diet (HFD) mice gradually increased compared with normal mice
Mice treated with licochalcone A weighed significantly less than HFD mice during the experiment stage (Figure 1B)
Summary
Obesity is becoming prevalent in developed and developing countries and is considered an important risk factor for chronic diseases including cardiovascular diseases, hypertension, osteoarthritis, some cancers, and diabetes [1]. Fatty liver disease is mainly divided into alcoholic fatty liver disease and nonalcoholic fatty liver disease (NAFLD). Some studies found that obesity was an important factor causing NAFLD and hepatic steatosis [2]. Most patients with NAFLD have metabolic diseases such as obesity, diabetes, and hyperlipidemia, and NAFLD can be divided into the nonalcoholic fatty liver and nonalcoholic steatohepatitis (NASH) stages according to the histology and disease development [3]. In the NASH stage, hepatic cells cause persistent inflammation, which leads to steatosis of the liver, chronic inflammation, and damage of hepatocytes [4]. If the patient does not adjust their diet and exercise properly, chronic inflammation of the liver would turn into liver cirrhosis or failure, and may even cause liver cancer
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