Abstract
Metabolic dysfunction-associated fatty liver disease (MAFLD) is a pathological accumulation of hepatic lipid closely linked with many metabolic disorders, oxidative stress and inflammation. We aimed to evaluate the hepatoprotective effect of bee bread on oxidative stress and inflammatory parameters in MAFLD rats. Twenty-eight male Sprague-Dawley rats were assigned into four groups (n = 7/group): normal control (NC), high-fat diet (HFD), bee bread (HFD + Bb, HFD + 0.5 g/kg/day bee bread) and orlistat (HFD + Or, HFD + 10 mg/kg/day orlistat) groups. After 12 weeks, the HFD group demonstrated significantly higher body weight gain, serum levels of lipids (TG, TC, LDL), liver enzymes (AST, ALT, ALP) and adiponectin, liver lipids (TG, TC) and insulin resistance (HOMA-IR). Furthermore, the HFD group showed significantly decreased antioxidant enzyme activities (GPx, GST, GR, SOD, CAT) and GSH level, and increased liver oxidative stress (TBARS, NO), translocation of Nrf2 to the nucleus, Keap1 expression and inflammation (TNF-α, NF-κβ, MCP-1) together with histopathological alterations (steatosis, hepatocyte hypertrophy, inflammatory cell infiltration, collagen deposition), which indicated the presence of non-alcoholic steatohepatitis (NASH) and fibrosis. Bee bread significantly attenuated all these changes exerted by HFD feeding. In conclusion, our results suggest that bee bread might have antioxidant, anti-inflammatory, anti-steatotic and anti-fibrotic effects that are beneficial in protecting liver progression towards NASH and fibrosis.
Highlights
Rats in the high-fat diet (HFD) group demonstrated significant increases in body weight gain, body mass index (BMI) and abdominal circumference (AC)/thoracic circumference (TC) ratio in comparison with the normal control (NC) group. All these parameters were distinctly decreased in the bee bread and orlistat groups except for the AC/TC ratio in the orlistat group compared with those of the HFD group
This study showed a significantly decreased serum level of adiponectin in the HFD group when compared with the NC group, whereas, the level of adiponectin was significantly increased after intake of bee bread
It is reported that TNF-α is involved in hepatic fatty acid synthesis, increases serum triglyceride level, activates the production of VLDL from the liver and stimulates both hepatocytes’ cell death and proliferation, is crucially involved in the pathogenesis of liver fibrosis [94]. This is confirmed by our present study in which significantly increased levels of pro-inflammatory mediators TNF-α and NF-κβ, and a significantly decreased level of anti-inflammatory cytokine IL-10 were observed in the liver of the HFD group, as well as elevation in serum lipids and the deposition of collagen fibers, which indicated the presence of liver fibrosis in this group
Summary
Non-alcoholic fatty liver disease (NAFLD) is identified as a variety of liver disorders ranging from hepatic steatosis (presence of macro-vesicular steatosis only) to non-alcoholic steatohepatitis (NASH) (presence of macro-vesicular steatosis with hepatocyte ballooning, lobular and/or portal inflammation and with/without fibrosis), progressing to advanced fibrosis, cirrhosis, and rarely, may develop into hepatocellular carcinoma [1]. It has been reported that the estimated worldwide prevalence of NAFLD is approximately 25% and this trend is predicted to increase yearly [2]. NAFLD is caused by an excessive intake of 4.0/). Alcoholic liver disease, which demonstrates similar hepatic disorders as NAFLD, is caused by an excessive intake of alcohol [3]
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