scholarly journals Propylthiouracil-Induced Liver Injury in Mice and the Protective Role of Taurine

2015 ◽  
Vol 21 (2) ◽  
pp. 94-101 ◽  
Author(s):  
Raziyeh Karamikhah ◽  
Akram Jamshidzadeh ◽  
Negar Azarpira ◽  
Arastoo Saeidi ◽  
Reza Heidari
Keyword(s):  
Liver Injury ◽  
Protective Role

A Protective Role of Okadaic Acid in Liver Injury Induced by Amoxicillin

2022 ◽  
Author(s):  
D. Li ◽  
W. Shi ◽  
X. Lu ◽  
Z. Liu ◽  
S. Zhang ◽  
...  
Keyword(s):  
Liver Injury ◽  
Okadaic Acid ◽  
Protective Role

scholarly journals Protective role of Ficus benghalensis against isoniazid-rifampicin induced oxidative liver injury in rat

2012 ◽  
Vol 22 (3) ◽  
pp. 604-610 ◽  
Author(s):  
S. Angala Parameswari ◽  
T. S. Mohamed Saleem ◽  
K. B Chandrasekar ◽  
C. Madhusudhana Chetty
Keyword(s):  
Liver Injury ◽  
Protective Role ◽  
Ficus Benghalensis

Protective role of antithrombin in mouse models of liver injury

2012 ◽  
Vol 57 (5) ◽  
pp. 980-986 ◽  
Author(s):  
José A. Guerrero ◽  
Raúl Teruel ◽  
Constantino Martínez ◽  
Isabel Arcas ◽  
Irene Martínez-Martínez ◽  
...  
Keyword(s):  
Liver Injury ◽  
Mouse Models ◽  
Protective Role

scholarly journals Protective Role of Estrogen-induced miRNA-29 Expression in Carbon Tetrachloride-induced Mouse Liver Injury

2012 ◽  
Vol 287 (18) ◽  
pp. 14851-14862 ◽  
Author(s):  
Yaqin Zhang ◽  
Linping Wu ◽  
Yang Wang ◽  
Mingcao Zhang ◽  
Limin Li ◽  
...  
Keyword(s):  
Carbon Tetrachloride ◽  
Liver Injury ◽  
Mouse Liver ◽  
Protective Role

scholarly journals Role of nitric oxide in hepatic microvascular injury elicited by acetaminophen in mice

2004 ◽  
Vol 286 (1) ◽  
pp. G60-G67 ◽  
Author(s):  
Yoshiya Ito ◽  
Edward R. Abril ◽  
Nancy W. Bethea ◽  
Robert S. McCuskey
Keyword(s):  
Nitric Oxide ◽  
Liver Injury ◽  
Cell Injury ◽  
Parenchymal Cell ◽  
Protective Role ◽  
Hepatic Expression ◽  
Inos Inhibitor ◽  
Microcirculatory Disturbances

Nitric oxide (NO) is suggested to play a role in liver injury elicited by acetaminophen (APAP). Hepatic microcirculatory dysfunction also is reported to contribute to the development of the injury. As a result, the role of NO in hepatic microcirculatory alterations in response to APAP was examined in mice by in vivo microscopy. A selective inducible NO synthase (iNOS) inhibitor,l- N6-(1-iminoethyl)-lysine (l-NIL), or a nonselective NOS inhibitor, NG-nitro-l-arginine methyl ester (l-NAME), was intraperitoneally administered to animals 10 min before APAP gavage. l-NIL suppressed raised alanine aminotransferase (ALT) values 6 h after APAP, whereas l-NAME increased those 1.7-fold. Increased ALT levels were associated with hepatic expression of iNOS. l-NIL, but not l-NAME, reduced the expression. APAP caused a reduction (20%) in the numbers of perfused sinusoids. l-NIL restored the sinusoidal perfusion, but l-NAME was ineffective. APAP increased the area occupied by infiltrated erythrocytes into the extrasinusoidal space. l-NIL tended to minimize this infiltration, whereas l-NAME further enhanced it. APAP caused an increase (1.5-fold) in Kupffer cell phagocytic activity. This activity in response to APAP was blunted by l-NIL, whereas l-NAME further elevated it. l-NIL suppressed APAP-induced decreases in hepatic glutathione levels. These results suggest that NO derived from iNOS contributes to APAP-induced parenchymal cell injury and hepatic microcirculatory disturbances. l-NIL exerts preventive effects on the liver injury partly by inhibiting APAP bioactivation. In contrast, NO derived from constitutive isoforms of NOS exerts a protective role in liver microcirculation against APAP intoxication and thereby minimizes liver injury.

scholarly journals Sophocarpine Attenuates LPS-Induced Liver Injury and Improves Survival of Mice through Suppressing Oxidative Stress, Inflammation, and Apoptosis

2018 ◽  
Vol 2018 ◽  
pp. 1-12 ◽  
Author(s):  
Zhengyu Jiang ◽  
Yan Meng ◽  
Lulong Bo ◽  
Changli Wang ◽  
Jinjun Bian ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Injury ◽  
Great Part ◽  
Protective Role ◽  
Stress Indicators ◽  
Oxidative Reaction ◽  
Hepatic Expression ◽  
Jnk Cascade ◽  
Oxidative Stress Indicators

Septic liver injury/failure that is mainly characterized by oxidative stress, inflammation, and apoptosis led to a great part of terminal liver pathology with limited effective intervention. Here, we used a lipopolysaccharide (LPS) stimulation model to simulate the septic liver injury and investigated the effect of sophocarpine on LPS-stimulated mice with endotoxemia. We found that sophocarpine increases the survival rate of mice and attenuates the LPS-induced liver injury, which is indicated by pathology and serum liver enzymes. Further research found that sophocarpine ameliorated hepatic oxidative stress indicators (H2O2, O2∙−, and NO) and enhanced the expression of antioxidant molecules such as superoxide dismutase (SOD), catalase (CAT), and glutathione (GSH). In addition, sophocarpine also attenuated regional and systematic inflammation and further reduced apoptosis of hepatocytes. Mechanistic evidence was also investigated in the present study as sophocarpine inhibited hepatic expression of the CYP2E/Nrf2 pathway during oxidative stress, inactivated p38/JNK cascade and NF-κB pathway, and, meanwhile, suppressed PI3K/AKT signaling that reduced apoptosis. Conclusively, the present study unveiled the protective role of sophocarpine in LPS-stimulated oxidative reaction, inflammation, and apoptosis by suppressing the CYP2E/Nrf2/ROS as well as PI3K/AKT pathways, suggesting its promising role in attenuating inflammation and liver injury of septic endotoxemia.

The protective role of Hepatopoietin Cn on liver injury induced by carbon tetrachloride in rats

2009 ◽  
Vol 39 (2) ◽  
pp. 200-206 ◽  
Author(s):  
Chun-Ping Cui ◽  
Ping Wei ◽  
Yang Liu ◽  
Da-Jin Zhang ◽  
Li-Sheng Wang ◽  
...  
Keyword(s):  
Carbon Tetrachloride ◽  
Liver Injury ◽  
Protective Role

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.

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