Abstract
The present study aimed to evaluate the potential synergistic and protective effects of ALM16, a mixture of Astragalus membranaceus (AM) and Lithospermum erythrorhizon (LE) extract in a ratio of 7 : 3, against hepatic steatosis in high fat diet (HFD)-induced nonalcoholic fatty liver disease (NAFLD) mice. Forty-eight mice were randomly divided into eight groups and orally administered daily for 6 weeks with a normal diet (ND) or high fat diet alone (HFD), HFD with AM (HFD + 100 mg/kg AM extract), HFD with LE (HFD + 100 mg/kg LE extract), HFD with ALM16 (HFD + 50, 100, and 200 mg/kg ALM16), or HFD with MT (HFD + 100 mg/kg Milk thistle extract) as a positive control. ALM16 significantly decreased the body and liver weight, serum and hepatic lipid profiles, including triglyceride (TG), total cholesterol (TC), high-density lipoprotein-cholesterol (HDL), and low-density lipoprotein-cholesterol (LDL), and serum glucose levels, compared to the HFD group. Moreover, ALM16 significantly ameliorated the HFD-induced increased hepatic injury markers, including aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), lactate dehydrogenase (LDH), and gamma-glutamyltransferase (GGT)-1. Furthermore, as compared to the mice fed HFD alone, ALM16 increased the levels of phosphorylated AMP-activated protein kinase (p-AMPK) and acetyl-CoA carboxylase (p-ACC), thereby upregulating the expression of carnitine palmitoyltransferase (CPT)-1 and downregulating the expression of sterol regulatory element-binding protein (SREBP)-1c and fatty acid synthase (FAS). These results demonstrated that ALM16 markedly inhibited HFD-induced hepatic steatosis in NAFLD mice by modulating AMPK and ACC signaling pathways, and may be more effective than the single extracts of AM or LE.
Highlights
Nonalcoholic fatty liver disease (NAFLD) is one of the common chronic liver diseases in metabolic syndrome, resulting from the hepatic lipid accumulation of >5% of liver weight [1]. e liver is the major contributor to whole-body lipogenesis, gluconeogenesis, and cholesterol metabolism [2, 3]. e development of NAFLD is characterized by abnormal liver function and can progress to more severe liver diseases such as nonalcoholic steatohepatitis (NASH), fibrosis, and cirrhosis [4, 5]
As compared to the mice fed high fat diet (HFD) alone, ALM16 increased the levels of phosphorylated AMP-activated protein kinase (p-AMPK) and acetyl-CoA carboxylase (p-ACC), thereby upregulating the expression of carnitine palmitoyltransferase (CPT)-1 and downregulating the expression of sterol regulatory element-binding protein (SREBP)-1c and fatty acid synthase (FAS). ese results demonstrated that ALM16 markedly inhibited HFD-induced hepatic steatosis in NAFLD mice by modulating AMPK and ACC signaling pathways, and may be more effective than the single extracts of Astragalus membranaceus (AM) or Lithospermum erythrorhizon (LE)
No significant differences in food intake were observed between the HFD group (2.8 g/day/mice) and all sample-treated groups (2.5–2.8 g/day/mice, Supplementary Figure 1)
Summary
Nonalcoholic fatty liver disease (NAFLD) is one of the common chronic liver diseases in metabolic syndrome, resulting from the hepatic lipid accumulation of >5% of liver weight [1]. e liver is the major contributor to whole-body lipogenesis, gluconeogenesis, and cholesterol metabolism [2, 3]. e development of NAFLD is characterized by abnormal liver function and can progress to more severe liver diseases such as nonalcoholic steatohepatitis (NASH), fibrosis, and cirrhosis [4, 5]. Nonalcoholic fatty liver disease (NAFLD) is one of the common chronic liver diseases in metabolic syndrome, resulting from the hepatic lipid accumulation of >5% of liver weight [1]. NAFLD has become a critical health concern worldwide owing to its increased morbidity and mortality. There are no approved agents currently available for the treatment of NAFLD [6]. NAFLD patients generally require long-term treatment, which can potentially induce serious or diverse side effects. Erefore, the identification of potential therapeutic compounds with better biological efficacy and safety, and fewer side effects is imperative [7]. The pathogenesis of NAFLD remained poorly understood; the ‘two-hit’ concept is generally recognized as the most important theory. Therapeutic strategies for NAFLD have focused on identifying potential agents that can exert effects to prevent hepatic steatosis and inflammation
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