Abstract

Allium victorialis L. (AVL) is a traditional medicinal plant recorded in the Compendium of Materia Medica (the Ming Dynasty). In general, it is used for hemostasis, analgesia, anti-inflammation, antioxidation, and to especially facilitate hepatoprotective effect. In recent years, it has received more and more attention due to its special nutritional and medicinal value. The present study investigates the effect and potential mechanism of AVL against alcoholic liver disease (ALD). C57BL/6 mice were fed Lieber–DeCarli liquid diet containing 5% ethanol plus a single ethanol gavage (5 g/kg), and followed up with the administration of AVL or silymarin. AML12 cells were stimulated with ethanol and incubated with AVL. AVL significantly reduced serum transaminase and triglycerides in the liver and attenuated histopathological changes caused by ethanol. AVL significantly inhibited SREBP1 and its target genes, regulated lipin 1/2, increased PPARα and its target genes, and decreased PPARγ expression caused by ethanol. In addition, AVL significantly enhanced FXR, LXRs, Sirt1, and AMPK expressions compared with the EtOH group. AVL also inhibited inflammatory factors, NLRP3, and F4/80 and MPO, macrophage and neutrophil markers. In vitro, AVL significantly reduced lipid droplets, lipid metabolism enzymes, and inflammatory factors depending on FXR activation. AVL could ameliorate alcoholic steatohepatitis, lipid deposition and inflammation in ALD by targeting FXR activation.

Highlights

  • Alcohol consumption is highly addictive and associated with social, economic, and multifarious health problems (GaliciaMoreno and Gutiérrez-Reyes, 2014)

  • Excessive alcohol consumption is responsible for the development of alcoholic liver disease (ALD), with a spectrum comprising alcoholic fatty liver, alcoholic steatohepatitis, and so on

  • The present study found that Allium victorialis L. (AVL) could attenuate ALD induced by Lieber–DeCarli liquid diet containing ethanol

Read more

Summary

Introduction

Alcohol consumption is highly addictive and associated with social, economic, and multifarious health problems (GaliciaMoreno and Gutiérrez-Reyes, 2014). Alcohol is first metabolized to acetaldehyde by alcohol dehydrogenase and partly metabolized by cytochrome P4502E1 (CYP2E1), catalase in hepatocyte microsomes and peroxisomes (Liu, 2014). This process would synthesize fatty acids, accumulate triglycerides (TGs) and further lead to fatty liver disease. Simple fatty liver is the early stage in ALD progression and would subsequently lead to steatosis, alcoholic hepatitis, fibrosis, and even cirrhosis with continuous consumption of excessive amounts of alcohol (Shearn et al, 2013; Addolorato et al, 2016). It is still critical to develop an effective therapeutic drug for ALD, which prevents progression and reduces fat deposition and accelerates regeneration and stability of hepatocytes and promotes liver activity

Methods
Results
Conclusion
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call