Tetrachlorobenzoquinone induces acute liver injury, up-regulates HO-1 and NQO1 expression in mice model: The protective role of chlorogenic acid

2014 ◽  
Vol 37 (3) ◽  
pp. 1212-1220 ◽  
Author(s):  
Demei Xu ◽  
Lihua Hu ◽  
Xiaomin Xia ◽  
Jianbo Song ◽  
Lingrui Li ◽  
...  
Keyword(s):  
Liver Injury ◽  
Chlorogenic Acid ◽  
Acute Liver Injury ◽  
Protective Role ◽  
Mice Model

scholarly journals Hepatic progenitor cells promote the repair of schistosomiasis liver injury by inhibiting IL-33 secretion in mice

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Beibei Zhang ◽  
Xiaoying Wu ◽  
Jing Li ◽  
An Ning ◽  
Bo Zhang ◽  
...  
Keyword(s):  
Liver Injury ◽  
Progenitor Cells ◽  
Normal Liver ◽  
Protective Role ◽  
Dependent Manner ◽  
Hepatic Progenitor Cells ◽  
Wild Type ◽  
Mice Model

Abstract Background Hepatic schistosomiasis, a chronic liver injury induced by long-term Schistosoma japonicum (S. japonicum) infection, is characterized by egg granulomas and fibrotic pathology. Hepatic progenitor cells (HPCs), which are nearly absent or quiescent in normal liver, play vital roles in chronic and severe liver injury. But their role in the progression of liver injury during infection remains unknown. Methods In this study, the hepatic egg granulomas, fibrosis and proliferation of HPCs were analyzed in the mice model of S. japonicum infection at different infectious stages. For validating the role of HPCs in hepatic injury, tumor necrosis factor-like-weak inducer of apoptosis (TWEAK) and TWEAK blocking antibody were used to manipulate the proliferation of HPCs in wild-type and IL-33−/− mice infected with S. japonicum. Results We found that the proliferation of HPCs was accompanied by inflammatory granulomas and fibrosis formation. HPCs expansion promoted liver regeneration and inhibited inflammatory egg granulomas, as well as the deposition of fibrotic collagen. Interestingly, the expression of IL-33 was negatively associated with HPCs’ expansion. There were no obvious differences of liver injury caused by infection between wild-type and IL-33−/− mice with HPCs’ expansion. However, liver injury was more attenuated in IL-33−/− mice than wild-type mice when the proliferation of HPCs was inhibited by anti-TWEAK. Conclusions Our data uncovered a protective role of HPCs in hepatic schistosomiasis in an IL-33-dependent manner, which might provide a promising progenitor cell therapy for hepatic schistosomiasis.

A protective role of IL-22BP in acute liver injury

2017 ◽  
Vol 66 (1) ◽  
pp. S333-S334
Author(s):  
D. Kleinschmidt ◽  
A.D. Giannou ◽  
J. Kempski ◽  
B. Steglich ◽  
F.J. Huber ◽  
...  
Keyword(s):  
Liver Injury ◽  
Acute Liver Injury ◽  
Protective Role

scholarly journals Hepatic Progenitor Cells Promote the Repair of Schistosomiasis Liver Injury Through Inhibiting IL-33 Secretion 

2021 ◽  
Author(s):  
Beibei Zhang ◽  
Xiaoying Wu ◽  
Jing Li ◽  
An Ning ◽  
Bo Zhang ◽  
...  
Keyword(s):  
Liver Injury ◽  
Progenitor Cells ◽  
Progenitor Cell ◽  
Normal Liver ◽  
Protective Role ◽  
Hepatic Progenitor Cells ◽  
Mice Model ◽  
Blocking Antibody

Abstract Background: Hepatic schistosomiasis, a chronic liver injury induced by long-term Schistosoma japonicum (S. japonicum) infection, is characterized by egg granulomas and fibrotic pathology. Hepatic progenitor cells (HPCs), which are nearly absent and quiescent in normal liver, play vital roles in chronic and severe liver injury. But their role in the progression of liver injury during infection remained unknown.Methods: In this study, the hepatic egg granulomas, fibrosis and proliferation of HPCs were analyzed in S. japonicum infection mice model at different infection stages. For validating the role of HPCs in hepatic injury, TNF­related weak inducer of apoptosis (TWEAK) and TWEAK blocking antibody were used to manipulate the proliferation of HPCs. Histologic pathology and the expression of IL-33 were examined. Results: We found that the proliferation of HPCs paralleled with inflammatory granulomas and fibrosis formation. Promoting HPCs expansion promote the liver regeneration and inhibit the hepatocytes injury, the inflammatory eggs granulomas and the deposition of fibrotic collagen. Interestingly, the expression of IL-33 decreased when HPCs were manipulated to proliferate. Thus, IL-33 might be involved in the liver repair dominated by HPCs. Conclusions: Collectively, our data uncovered a protective role of HPCs in hepatic schistosomiasis in an IL-33 related manner, which might provide a promising progenitor cell therapy for hepatic schistosomiasis.

scholarly journals Novel Protective Role of Nicotinamide Phosphoribosyltransferase in Acetaminophen-Induced Acute Liver Injury in Mice

2018 ◽  
Vol 188 (7) ◽  
pp. 1640-1652 ◽  
Author(s):  
Li Q. Zhang ◽  
Marianne Nsumu ◽  
Peixin Huang ◽  
Daniel P. Heruth ◽  
Sean M. Riordan ◽  
...  
Keyword(s):  
Liver Injury ◽  
Acute Liver Injury ◽  
Protective Role ◽  
Nicotinamide Phosphoribosyltransferase

Protective role of c‐Jun N‐terminal kinase‐2 (JNK2) in ibuprofen‐induced acute liver injury

2018 ◽  
Author(s):  
Miguel E Zoubek ◽  
Marius M Woitok ◽  
Svenja Sydor ◽  
Leonard J Nelson ◽  
Lars P Bechmann ◽  
...  
Keyword(s):  
Liver Injury ◽  
Acute Liver Injury ◽  
Protective Role

scholarly journals Cannabidiol Rescues Acute Hepatic Toxicity and Seizure Induced by Cocaine

2015 ◽  
Vol 2015 ◽  
pp. 1-12 ◽  
Author(s):  
Luciano Rezende Vilela ◽  
Lindisley Ferreira Gomides ◽  
Bruna Araújo David ◽  
Maísa Mota Antunes ◽  
Ariane Barros Diniz ◽  
...  
Keyword(s):  
Liver Injury ◽  
Liver Damage ◽  
Acute Liver Injury ◽  
Endocannabinoid System ◽  
Protective Role ◽  
Acute Liver Damage ◽  
Protective Actions ◽  
Cocaine Toxicity ◽  
Hepatotoxic Drug

Cocaine is a commonly abused illicit drug that causes significant morbidity and mortality. The most severe and common complications are seizures, ischemic strokes, myocardial infarction, and acute liver injury. Here, we demonstrated that acute cocaine intoxication promoted seizure along with acute liver damage in mice, with intense inflammatory infiltrate. Considering the protective role of the endocannabinoid system against cell toxicity, we hypothesized that treatment with an anandamide hydrolysis inhibitor, URB597, or with a phytocannabinoid, cannabidiol (CBD), protects against cocaine toxicity. URB597 (1.0 mg/kg) abolished cocaine-induced seizure, yet it did not protect against acute liver injury. Using confocal liver intravital microscopy, we observed that CBD (30 mg/kg) reduced acute liver inflammation and damage induced by cocaine and prevented associated seizure. Additionally, we showed that previous liver damage induced by another hepatotoxic drug (acetaminophen) increased seizure and lethality induced by cocaine intoxication, linking hepatotoxicity to seizure dynamics. These findings suggest that activation of cannabinoid system may have protective actions on both liver and brain induced by cocaine, minimizing inflammatory injury promoted by cocaine, supporting its further clinical application in the treatment of cocaine abuse.

scholarly journals The role of non-steroidal anti-inflammatory drugs in acute liver injury.

BMJ ◽  
1992 ◽  
Vol 305 (6858) ◽  
pp. 865-868 ◽  
Author(s):  
L. A. Garcia Rodriguez ◽  
S. Perez Gutthann ◽  
A. M. Walker ◽  
L. Lueck
Keyword(s):  
Liver Injury ◽  
Acute Liver Injury ◽  
Inflammatory Drugs ◽  
Anti Inflammatory
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