Abstract
An effective treatment for non-alcoholic fatty liver disease (NAFLD) is urgently needed. In the present study, we investigated whether the Chinese medicine Chai Hu Li Zhong Tang (CHLZT) could protect against the development of NAFLD. Rats in an animal model of NAFLD were treated with CHLZT, and their serum levels of cholesterol (TC), triglycerides (TG), high density lipoprotein-cholesterol (HDL-C), low density lipoprotein-cholesterol (LDL-C), aspartate aminotransferase (AST), and alanine aminotransferase (ALT) were detected with an automatic biochemical analyzer. A cellular model of NAFLD was also established by culturing HepG2 cells in a medium that contained a long chain fat emulsion. Those cells were treated with CHLZT that contained serum from rats. After treatment, the levels of adenylate-activated protein kinase (AMPK) α (AMPKα), p-AMPKα, acetyl coenzyme A carboxylase (ACC) α (ACCα), pACCα, PPARγ, and SREBP-2 were detected. The AMPK agonist, acadesine (AICAR), was used as a positive control compound. Our results showed that CHLZT or AICAR significantly decreased the serum levels of TG, TC, LDL-C, AST, ALT, and insulin in NAFLD rats, and significantly increased their serum HDL-C levels. Treatments with CHLZT or AICAR significantly decreased the numbers of lipid droplets in NAFLD liver tissues and HepG2 cells. CHLZT and AICAR increased the levels of p-AMPKα and PPARγ in the NAFLD liver tissues and HepG2 cells, but decreased the levels of ACC-α, p-ACC-α, SREBP-2, and 3-hydroxyl-3-methylglutaryl-coenzyme A reductase (HMGR). CHLZT protects against NAFLD by activating AMPKα, and also by inhibiting ACC activity, down-regulating SREBP2 and HMGR, and up-regulating PPAR-γ. Our results suggest that CHLZT might be useful for treating NAFLD in the clinic.
Highlights
Non-alcoholic fatty liver disease (NAFLD) is a clinical syndrome characterized by hepatocellular steatosis, cellular injury, and the infiltration of inflammatory cells into the liver tissues of individuals without a history of excessive drinking [1,2]
To evaluate our NAFLD rat model and the effects of Chai Hu Li Zhong Tang (CHLZT), we detected the levels of TG, TC, high density lipoprotein-cholesterol (HDL-C), low density lipoprotein-cholesterol (LDL-C), alanine aminotransferase (ALT), aspartate aminotransferase (AST), and insulin in the model rats (Figure 1)
We treated NAFLD rats with CHLZT and analyzed their blood’s biochemical parameters to determine how the affects produced by CHLZT might be related to adenylate-activated protein kinase (AMPK), peroxisome proliferator activated receptors (PPAR)-γ, SREBP2, and signaling
Summary
Non-alcoholic fatty liver disease (NAFLD) is a clinical syndrome characterized by hepatocellular steatosis, cellular injury, and the infiltration of inflammatory cells into the liver tissues of individuals without a history of excessive drinking [1,2]. Epidemiological studies indicate that the prevalence of NAFLD has surpassed those of viral hepatitis and alcoholic liver disease (ALD), making it the world’s most commonly diagnosed medical and social problem [3]. In Japan, the prevalence of NAFLD has increased 3–20-fold, and exceeds that of hepatitis C. The early clinical manifestation of NAFLD is mainly simple fatty liver, which is characterized by liver steatosis and an accumulation of triglycerides (TGs) in liver tissue [4,5]
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