Abstract
Silybin, a natural antioxidant, has been traditionally used against a variety of liver ailments. To investigate its effect and the underlying mechanisms of action on non-alcoholic fatty liver in rats, we used 60 4-6-week-old male Sprague-Dawley rats to establish fatty liver models by feeding a high-fat diet for 6 weeks. Hepatic enzyme, serum lipid levels, oxidative production, mitochondrial membrane fluidity, homeostasis model assessment-insulin resistance index (HOMA-IR), gene and protein expression of adiponectin, and resistin were evaluated by biochemical, reverse transcription polymerase chain reaction (RT-PCR) and Western blot analysis. Compared with the model group, silybin treatment (26.25 mg·kg(-1)·day(-1), started at the beginning of the protocol) significantly protected against high-fat-induced fatty liver by stabilizing mitochondrial membrane fluidity, reducing serum content of alanine aminotransferase (ALT) from 450 to 304 U/L, decreasing hepatic malondialdehyde (MDA) from 1.24 to 0.93 nmol/mg protein, but increasing superoxide dismutase (SOD) and glutathione (GSH) levels from 8.03 to 9.31 U/mg protein and from 3.65 to 4.52 nmol/mg protein, respectively. Moreover, silybin enhanced the gene and protein expression of adiponectin from 215.95 to 552.40, but inhibited that of resistin from 0.118 to 0.018. Compared to rosiglitazone (0.5 mg·kg(-1)·day(-1), started at the beginning of the protocol), silybin was effective in stabilizing mitochondrial membrane fluidity, reducing SOD as well as ALT, and regulating gene and protein expression of adiponectin (P < 0.05). These results suggest that mitochondrial membrane stabilization, oxidative stress inhibition, as well as improved insulin resistance, may be the essential mechanisms for the hepatoprotective effect of silybin on non-alcoholic fatty liver disease in rats. Silybin was more effective than rosiglitazone in terms of maintaining mitochondrial membrane fluidity and reducing oxidative stress.
Highlights
Non-alcoholic fatty liver disease (NAFLD), strongly associated with insulin resistance and metabolic syndrome [1,2], is one of the common liver diseases affecting at least 24-42% of adults in the Western population [3] and 5-40% in the Asia-Pacific region [3,4]
We focused on insulin resistance and hepatic expression of adipocytokines in NAFLD models and on how they changed with the use of silybin and rosiglitazone
We proposed to evaluate the effects of non-complex silybin on animal models of NAFLD induced by a high-fat diet for 6 weeks, in order to determine the probable mechanisms of action of this agent, and to compare its effect to that of the insulin sensitizer thiazolidinedione
Summary
Non-alcoholic fatty liver disease (NAFLD), strongly associated with insulin resistance and metabolic syndrome [1,2], is one of the common liver diseases affecting at least 24-42% of adults in the Western population [3] and 5-40% in the Asia-Pacific region [3,4]. NAFLD represents a spectrum of liver disorders ranging from simple steatosis to non-alcoholic steatohepatitis (NASH) and advanced hepatic fibrosis or even cirrhosis [5]. 12-24% of patients with simple steatosis are estimated to develop NASH after 8-13 years. NAFLD is considered to be one of the clinical features of metabolic syndrome in which insulin resistance plays a key role [7,8]. Adipose tissue has emerged as an endocrine organ producing adipocytokines, which play a central role in energy homeostasis and have an essential effect on the pathogenesis and progress of NAFLD [11]. We focused on insulin resistance and hepatic expression of adipocytokines in NAFLD models and on how they changed with the use of silybin and rosiglitazone
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