Pueraria Extract Ameliorates Alcoholic Liver Disease via the Liver–Gut–Brain Axis: Focus on Restoring the Intestinal Barrier and Inhibiting Alcohol Metabolism

Oct 24, 2024Journal of agricultural and food chemistry

Pueraria Extract May Improve Alcoholic Liver Disease by Protecting the Gut Barrier and Slowing Alcohol Breakdown Through the Liver-Gut-Brain System

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Abstract

Pueraria extract (PUE) reduced serum levels of ALT, AST, TC, and TG in models of alcoholic liver disease.

PUE treatment decreased inflammatory markers and alleviated liver inflammation.
Gene expression of ADH1 was reduced, leading to lower serum levels of acetaldehyde, which is produced during alcohol metabolism.
PUE increased the gene expression of ALDH2, promoting the breakdown of acetaldehyde.
PUE altered gut microbiota composition, reducing harmful bacteria and lipopolysaccharide production.
Fecal microbiota transplantation confirmed that PUE's effects on ALD were dependent on gut microbiota changes.
PUE may regulate gut microbiota and inhibit ethanol metabolism to alleviate alcoholic liver disease.

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Alcoholic liver disease (ALD) is one of the causes of hepatocellular carcinoma, accompanied by intestinal leakage and microbial changes. Pueraria has protective effects on liver injury. The aim of this study was to investigate the mechanism of pueraria in the treatment of ALD. UPLC-Q/TOF-MS was used to analyze the composition of the pueraria extract (PUE). Acute and chronic ALD models were established to evaluate the antialcoholic and hepatoprotective effects of PUE. As a result, PUE treatment reduced the serum levels of ALT, AST, TC, and TG and inflammatory factors and alleviated liver inflammation and drunk state. PUE decreased the gene expression of ADH1 and the serum level of acetaldehyde (ACH) to inhibit the generation of ACH from ethanol metabolism, increased the gene level of ALDH2 to accelerate the decomposition of ACH, and thereby alleviated liver inflammation and intestinal barrier damage. Meanwhile, 16 S rDNA revealed that PUE altered the microbiota composition, reduced the amount ofand, and thus inhibited the generation of lipopolysaccharide and its downstream-like TLR4/MyD88/NF-κB pathway. PUE also increased the abundance of,, andand producted short-chain fatty acids to protect the intestinal wall. Treatment with fecal microbiota transplantation further confirmed that PUE gut microbiota dependently alleviated ALD. Therefore, PUE regulated gut microbiota and inhibited ethanol metabolism to alleviate ALD through the liver-gut-brain axis. It has good prospects in the future. Proteobacteria Desulfobacterota Bacteroides Ruminococcus Prevotella

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