Tamarixetin: A Promising Bioflavonoid Against Acetaminophen-Induced Liver Injury

Oxidative stress, mitochondrial dysfunction, and inflammatory responses cause acute liver failure in most cases of acetaminophen (APAP) overdose. Tamarixetin (Trx), an antioxidant and anti-inflammatory flavonoid, has not yet been studied in models of APAP-induced hepatotoxicity. Trx was tested for i...

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Main Authors: Mehmet Ali Telafarlı, Ejder Saylav Bora, Firdes Topal, Oytun Erbaş
Format: Article
Language:English
Published: MDPI AG 2025-07-01
Series:Current Issues in Molecular Biology
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Online Access:https://www.mdpi.com/1467-3045/47/7/524
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author Mehmet Ali Telafarlı
Ejder Saylav Bora
Firdes Topal
Oytun Erbaş
author_facet Mehmet Ali Telafarlı
Ejder Saylav Bora
Firdes Topal
Oytun Erbaş
author_sort Mehmet Ali Telafarlı
collection DOAJ
description Oxidative stress, mitochondrial dysfunction, and inflammatory responses cause acute liver failure in most cases of acetaminophen (APAP) overdose. Tamarixetin (Trx), an antioxidant and anti-inflammatory flavonoid, has not yet been studied in models of APAP-induced hepatotoxicity. Trx was tested for its protective effects on APAP-induced liver injury in rats using biochemical, histopathological, and oxidative stress parameters. Three groups of 30 male Wistar rats were randomly assigned to the following groups: control, APAP + Saline, and APAP + Trx (3 mg/kg/day, intraperitoneally for 3 days). A single 300 mg/kg intraperitoneal APAP dose caused hepatotoxicity. ALT, MDA, GSH, HSP-70, and thioredoxin were measured in blood and liver tissues. Liver sections were histopathologically examined. APAP depleted hepatic GSH and Trx and increased serum ALT and MDA. Trx treatment significantly reduced ALT (201.2 → 105.1 U/L), MDA (5.5 → 3.4 nmol/mg), and the percentage of histologically damaged hepatocytes (58.5% → 9.5%), while restoring GSH and thioredoxin levels. Notably, HSP-70 expression exceeded that of APAP and control levels, suggesting the modulation of the stress response. The Trx group showed significant hepatoprotection histologically. Trx reduces APAP-induced hepatic damage, likely through antioxidant and anti-inflammatory mechanisms. These findings suggest that Trx may be a natural hepatoprotectant, warranting clinical trials.
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spelling doaj-art-58e002b8dceb48ea835f9fa3c9a6c9222025-08-20T03:07:54ZengMDPI AGCurrent Issues in Molecular Biology1467-30371467-30452025-07-0147752410.3390/cimb47070524Tamarixetin: A Promising Bioflavonoid Against Acetaminophen-Induced Liver InjuryMehmet Ali Telafarlı0Ejder Saylav Bora1Firdes Topal2Oytun Erbaş3Department of Emergency Medicine, Erzurum City Hospital, 25240 Erzurum, TurkeyDepartment of Emergency Medicine, Faculty of Medicine, Izmir Katip Çelebi University, 35360 Izmir, TurkeyDepartment of Gastroenterology, Faculty of Medicine, Izmir Katip Çelebi University, 35360 Izmir, TurkeyBiruni Research Center (BAMER), Faculty of Medicine, Biruni University, 34015 Istanbul, TurkeyOxidative stress, mitochondrial dysfunction, and inflammatory responses cause acute liver failure in most cases of acetaminophen (APAP) overdose. Tamarixetin (Trx), an antioxidant and anti-inflammatory flavonoid, has not yet been studied in models of APAP-induced hepatotoxicity. Trx was tested for its protective effects on APAP-induced liver injury in rats using biochemical, histopathological, and oxidative stress parameters. Three groups of 30 male Wistar rats were randomly assigned to the following groups: control, APAP + Saline, and APAP + Trx (3 mg/kg/day, intraperitoneally for 3 days). A single 300 mg/kg intraperitoneal APAP dose caused hepatotoxicity. ALT, MDA, GSH, HSP-70, and thioredoxin were measured in blood and liver tissues. Liver sections were histopathologically examined. APAP depleted hepatic GSH and Trx and increased serum ALT and MDA. Trx treatment significantly reduced ALT (201.2 → 105.1 U/L), MDA (5.5 → 3.4 nmol/mg), and the percentage of histologically damaged hepatocytes (58.5% → 9.5%), while restoring GSH and thioredoxin levels. Notably, HSP-70 expression exceeded that of APAP and control levels, suggesting the modulation of the stress response. The Trx group showed significant hepatoprotection histologically. Trx reduces APAP-induced hepatic damage, likely through antioxidant and anti-inflammatory mechanisms. These findings suggest that Trx may be a natural hepatoprotectant, warranting clinical trials.https://www.mdpi.com/1467-3045/47/7/524tamarixetinacetaminophenhepatotoxicityoxidative stressliver protection
spellingShingle Mehmet Ali Telafarlı
Ejder Saylav Bora
Firdes Topal
Oytun Erbaş
Tamarixetin: A Promising Bioflavonoid Against Acetaminophen-Induced Liver Injury
Current Issues in Molecular Biology
tamarixetin
acetaminophen
hepatotoxicity
oxidative stress
liver protection
title Tamarixetin: A Promising Bioflavonoid Against Acetaminophen-Induced Liver Injury
title_full Tamarixetin: A Promising Bioflavonoid Against Acetaminophen-Induced Liver Injury
title_fullStr Tamarixetin: A Promising Bioflavonoid Against Acetaminophen-Induced Liver Injury
title_full_unstemmed Tamarixetin: A Promising Bioflavonoid Against Acetaminophen-Induced Liver Injury
title_short Tamarixetin: A Promising Bioflavonoid Against Acetaminophen-Induced Liver Injury
title_sort tamarixetin a promising bioflavonoid against acetaminophen induced liver injury
topic tamarixetin
acetaminophen
hepatotoxicity
oxidative stress
liver protection
url https://www.mdpi.com/1467-3045/47/7/524
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AT firdestopal tamarixetinapromisingbioflavonoidagainstacetaminopheninducedliverinjury
AT oytunerbas tamarixetinapromisingbioflavonoidagainstacetaminopheninducedliverinjury