Imatinib-induced hepatotoxicity via oxidative stress and activation of NLRP3 inflammasome: an in vitro and in vivo study

Imatinib (IM), a milestone drug used in the field of molecular targeted therapy, has been reported to cause serious adverse liver effects, including liver failure and even death. Immune-mediated injury and mitochondrial dysfunction are involved in drug-induced liver injury. However, the mechanism of...

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Veröffentlicht in:Archives of toxicology 2022-04, Vol.96 (4), p.1075-1087
Hauptverfasser: Huang, Feng-Ru, Fang, Wen-Tong, Cheng, Zi-Ping, Shen, Ye, Wang, Dun-Jian, Wang, Yong-Qing, Sun, Lu-Ning
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container_issue 4
container_start_page 1075
container_title Archives of toxicology
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creator Huang, Feng-Ru
Fang, Wen-Tong
Cheng, Zi-Ping
Shen, Ye
Wang, Dun-Jian
Wang, Yong-Qing
Sun, Lu-Ning
description Imatinib (IM), a milestone drug used in the field of molecular targeted therapy, has been reported to cause serious adverse liver effects, including liver failure and even death. Immune-mediated injury and mitochondrial dysfunction are involved in drug-induced liver injury. However, the mechanism of IM-induced hepatotoxicity remains unclear and warrants further study. In our study, Sprague Dawley rats were administered IM by gavage with 50 mg/kg body weight (BW) once daily for 10 days. Drug-induced liver injury accompanied by inflammatory infiltration was observed in rats following IM exposure, and the expression of NOD-like receptor protein 3 (NLRP3) inflammasome-related proteins was significantly increased compared with that of the control. HepG2 cells were exposed to 0–100 μM IM for 24 h. The results showed that IM decreased cell viability in a dose-dependent manner. Moreover, IM induced a state of obvious oxidative stress and activation of nuclear factor kappa B (NF-κB) in cells, which resulted in the activation of NLRP3 inflammasomes, including caspase 1 cleavage and IL-1β release. These results were significantly reduced after the use of the antioxidants N-acetyl-l-cysteine or the NF-κB inhibitor pyrrolidine di-thio-carbamate. Furthermore, NLRP3 knockdown significantly reduced the release of inflammatory cytokines and improved cell viability. In summary, our data demonstrated that oxidative stress and NLRP3 inflammasome activation are involved in the process of IM-induced hepatotoxicity. The results of this study provide a reference for the prevention and treatment of IM-induced hepatotoxicity.
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Immune-mediated injury and mitochondrial dysfunction are involved in drug-induced liver injury. However, the mechanism of IM-induced hepatotoxicity remains unclear and warrants further study. In our study, Sprague Dawley rats were administered IM by gavage with 50 mg/kg body weight (BW) once daily for 10 days. Drug-induced liver injury accompanied by inflammatory infiltration was observed in rats following IM exposure, and the expression of NOD-like receptor protein 3 (NLRP3) inflammasome-related proteins was significantly increased compared with that of the control. HepG2 cells were exposed to 0–100 μM IM for 24 h. The results showed that IM decreased cell viability in a dose-dependent manner. Moreover, IM induced a state of obvious oxidative stress and activation of nuclear factor kappa B (NF-κB) in cells, which resulted in the activation of NLRP3 inflammasomes, including caspase 1 cleavage and IL-1β release. These results were significantly reduced after the use of the antioxidants N-acetyl-l-cysteine or the NF-κB inhibitor pyrrolidine di-thio-carbamate. Furthermore, NLRP3 knockdown significantly reduced the release of inflammatory cytokines and improved cell viability. In summary, our data demonstrated that oxidative stress and NLRP3 inflammasome activation are involved in the process of IM-induced hepatotoxicity. 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subjects Animals
Antioxidants
Biomedical and Life Sciences
Biomedicine
Body weight
Caspase-1
Cell viability
Chemical and Drug Induced Liver Injury - etiology
Cytokines
Environmental Health
Hepatotoxicity
IL-1β
Imatinib
Imatinib Mesylate - pharmacology
In vivo methods and tests
Inflammasomes
Inflammation
Injuries
Liver
Liver diseases
Mitochondria
N-Acetyl-L-cysteine
NF-kappa B - metabolism
NF-κB protein
NLR Family, Pyrin Domain-Containing 3 Protein - metabolism
NLR Proteins - metabolism
Occupational Medicine/Industrial Medicine
Organ Toxicity and Mechanisms
Oxidative Stress
Pharmacology/Toxicology
Proteins
Pyrrolidine
Rats
Rats, Sprague-Dawley
title Imatinib-induced hepatotoxicity via oxidative stress and activation of NLRP3 inflammasome: an in vitro and in vivo study
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