Abstract
Non-alcoholic fatty liver disease (NAFLD) has become a common liver disease in recent decades. No effective treatment is currently available. Probiotics and natural functional food may be promising therapeutic approaches to this disease. The present study aims to investigate the efficiency of the anthraquinone from Cassia obtusifolia L. (AC) together with cholesterol-lowering probiotics (P) to improve high-fat diet (HFD)-induced NAFLD in rat models and elucidate the underlying mechanism. Cholesterol-lowering probiotics were screened out by MRS-cholesterol broth with ammonium ferric sulfate method. Male Sprague–Dawley rats were fed with HFD and subsequently administered with AC and/or P. Lipid metabolism parameters and fat synthesis related genes in rat liver, as well as the diversity of gut microbiota were evaluated. The results demonstrated that, compared with the NAFLD rat, the serum lipid levels of treated rats were reduced effectively. Besides, cholesterol 7α-hydroxylase (CYP7A1), low density lipoprotein receptor (LDL-R) and farnesoid X receptor (FXR) were up-regulated while the expression of 3-hydroxy-3-methyl glutaryl coenzyme A reductase (HMGCR) was reduced. The expression of peroxisome proliferator activated receptor (PPAR)-α protein was significantly increased while the expression of PPAR-γ and sterol regulatory element binding protein-1c (SREBP-1c) was down-regulated. In addition, compared with HFD group, in AC, P and AC+P group, the expression of intestinal tight-junction protein occludin and zonula occluden-1 (ZO-1) were up-regulated. Furthermore, altered gut microbiota diversity after the treatment of probiotics and AC were analysed. The combination of cholesterol-lowering probiotics and AC possesses a therapeutic effect on NAFLD in rats by up-regulating CYP7A1, LDL-R, FXR mRNA and PPAR-α protein produced in the process of fat metabolism while down-regulating the expression of HMGCR, PPAR-γ and SREBP-1c, and through normalizing the intestinal dysbiosis and improving the intestinal mucosal barrier function.
Highlights
With the prevalence of obesity, hyperlipidemia, type II diabetes, and metabolic syndrome, the morbidity of nonalcoholic fatty liver disease (NAFLD) is constantly rising worldwide [1]
Recent studies indicate that about 50% of NAFLD patients may develop into non-alcoholic steatohepatitis (NASH) and 40% may progress to liver fibrosis after 4–13 years [2]
NAFLD patients are usually accompanied with obesity and insulin resistance, but not all obese people develop into NAFLD, the intestinal factors may play a key role in the pathogenesis of NAFLD [3]
Summary
With the prevalence of obesity, hyperlipidemia, type II diabetes, and metabolic syndrome, the morbidity of nonalcoholic fatty liver disease (NAFLD) is constantly rising worldwide [1]. Recent studies indicate that about 50% of NAFLD patients may develop into non-alcoholic steatohepatitis (NASH) and 40% may progress to liver fibrosis after 4–13 years [2]. NAFLD patients are usually accompanied with obesity and insulin resistance, but not all obese people develop into NAFLD, the intestinal factors may play a key role in the pathogenesis of NAFLD [3]. Studies have shown that the lipopolysaccharide (LPS) of gram-negative bacteria in the intestine can be transported to the liver through the portal vein. A large amount of Gram-negative bacteria may over proliferate and produce endotoxins, results in metabolic disorders, obesity, diabetes, NALD and NASH [4]. Since the intestinal microbiota is closely related to obesity, insulin resistance, NAFLD and NASH, it is possible to prevent the occurrence of NAFLD by adjusting the intestinal microbial structure
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