Prospective Application of Tannic Acid in Acetaminophen (APAP)-Induced Acute Liver Failure

This study investigated the effect of tannic acid (TA), a natural plant-derived polyphenol, on hepatocyte viability and function, focusing on both hepatoprotective and hepatocurative aspects within liver failure models. In an in vitro prevention model, the TA-containing group exhibited 1.5-fold and...

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Published in:International journal of molecular sciences 2023-12, Vol.25 (1), p.317
Main Authors: Lin, Yong-Heng, Lin, Yu-Che, Hou, Yung-Te
Format: Article
Language:English
Subjects:
Acetaminophen
acetaminophen-induced liver injury
Albumin
Analgesics
Antioxidants
Aspartate
Bilirubin
Comparative analysis
Gene expression
hepatoprotective and hepatocurative
Herbal medicine
Liver
Liver failure
liver regeneration
Metabolism
Metabolites
Oxidative stress
tannic acid
Toxicity
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Summary:This study investigated the effect of tannic acid (TA), a natural plant-derived polyphenol, on hepatocyte viability and function, focusing on both hepatoprotective and hepatocurative aspects within liver failure models. In an in vitro prevention model, the TA-containing group exhibited 1.5-fold and 59-fold higher relative cell viability and albumin synthesis, respectively, in injured mature hepatocytes (MHs) and 1.14-fold and 1.10-fold higher values in injured small hepatocytes (SHs), compared with the TA-free group. In the in vitro curative model, the TA-containing group exhibited 3.25-fold and 113-fold higher relative cell viability and albumin synthesis, respectively, in injured MHs and 0.36-fold and 3.55-fold higher values in injured SHs, compared with the TA-free group. In the in vivo disease model, the administration of 300 μL of 1 μg/mL TA significantly mitigated acute liver failure damage and post-APAP toxicity in mice. This was evident in serum analysis, where the levels of alanine transaminase, aspartate aminotransferase, and total bilirubin notably decreased, in agreement with histological observations. The study findings reveal that TA can enhance hepatic function at specific additive concentrations. Furthermore, even when injured by APAP, hepatocytes could revert to their preinjury state after additional TA supplementation. Additionally, pretreating hepatocytes with TA can alleviate subsequent damage. Thus, TA holds clinical potential in the treatment of APAP-induced liver failure.
ISSN:1422-0067
1661-6596
1422-0067
DOI:10.3390/ijms25010317