Abstract
Context: Alcoholic liver fibrosis (ALF) is treatable and reversible consequence of liver disease. Intestinal microflora plays an important role in the progression of liver disease. Garlic (Allium sativum L. [Amaryllidaceae]) has been consumed as a traditional medicine to treat liver injury.Objective: To investigate the effects of garlic polysaccharide (GP) on ALF and intestinal microflora in mice.Materials and methods: KM mice were orally administered with alcohol (56%, 6 mL/kg) for 30 d to establish ALF model, and divided into four groups together with control group (water only). Hugan tablet (60 mg/kg) or GP (250 and 150 mg/kg) were given 5 h after each dose of alcohol. Biochemical markers in serum and liver homogenate were determined with kits. Alteration of intestinal microflora, and protein expressions of TGF-β1, TNF-α and decorin were detected.Results: In GP-H group, ALT and AST decreased to 18.85 ± 4.71 U/L and 40.84 ± 7.89 U/L. MDA, TC, TG and LDL-C decreased to 2.32 ± 0.86 mmol/mg, 0.21 ± 0.12 mmol/L, 0.96 ± 0.31 mmol/L and 0.084 ± 0.027 mmol/L. SOD, GSH-Px and GSH increased to 118.32 ± 16.32 U/mg, 523.72 ± 64.20 U/mg and 0.56 ± 0.05 mg/g. Ratios of TGF-β1 and TNF-α decreased to 0.608 ± 0.170 and 1.057 ± 0.058, decorin increased to 2.182 ± 0.129. Lachnospiraceae and Lactobacillus increased, Facklamia and Firmicutes decreased with GP pretreatment.Discussion and conclusions: Intestinal microflora provides novel insight into the mechanisms of GP that may be used to treat ALF and intestinal microflora dysbiosis.
Highlights
Alcoholic liver disease (ALD) is a major cause of morbidity and mortality (Cho et al 2017), and affects millions of individuals worldwide
HPLC profile indicated that garlic polysaccharide (GP) had a single and symmetrically sharp peak (Figure 1(B)), revealing that GP was a homogeneous polysaccharide with a purity of 98% by area normalization method
Under alcoholic liver fibrosis (ALF), the quiescent hepatic stellate cells (HSCs) trans-differentiate into fibrogenic myofibroblast-like cells caused by platelet-derived growth factor (PDGF), tumour necrosis factor-a (TNF-a), Transforming growth factor-b1 (TGF-b1) or reactive oxygen species (ROS) (Dong et al 2015), with expression of a-smooth muscle actin and type I collagen, and secreting profibrogenic mediators, promoting the progression of liver fibrosis (Bai et al 2016)
Summary
Alcoholic liver disease (ALD) is a major cause of morbidity and mortality (Cho et al 2017), and affects millions of individuals worldwide. The development of ALD involves some steps, which include alcoholic steatosis, alcoholic hepatitis, alcoholic liver fibrosis (ALF), alcoholic cirrhosis and liver cancer (Chuang et al 2016). ALF develops from simple steatosis and hepatitis to cirrhosis and even liver cancer (Baghy et al 2012). It is treatable and potentially reversible consequence of liver disease (Lee and Friedman 2010), and the effective antifibrotic methods significantly alter the management and prognosis of patients with liver disease (Friedman 2003). Transforming growth factor-b1 (TGF-b1) increases the accumulation of these matrix proteins at the injury site and promotes fibrosis (Goetsch and Niesler 2016), whereas the proteoglycan decorin acts as an anti-fibrotic agent via the binding and neutralization of TGF-b1.
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