Mechanism of Cyclosporin A- and Phalloidin-induced Liver Injury: Experimental Studies on Hepatic Bilirubin Transport

1989 ◽  
Vol 8 (2) ◽  
pp. 155-156
Author(s):  
G. Nassuato ◽  
M. Strazzabosco ◽  
M. Muraca ◽  
D. Passera ◽  
A. Fragasso ◽  
...  
Keyword(s):  
Liver Injury ◽  
Cyclosporin A ◽  
Experimental Studies

Mesenchymal Stem Cell Therapy for Acetaminophen-Related Liver Injury: A Systematic Review and Meta-Analysis of Experimental Studies in Vivo

2021 ◽  
Vol 16 ◽  
Author(s):  
Li Wang ◽  
Yiwen Zhang ◽  
Jiajun Zhong ◽  
Yuan Zhang ◽  
Shuisheng Zhou ◽  
...  
Keyword(s):  
Systematic Review ◽  
Stem Cell ◽  
Liver Injury ◽  
Mesenchymal Stem Cell ◽  
Small Sample Size ◽  
Meta Analysis ◽  
Experimental Studies ◽  
Small Sample ◽  
Control Group

Objective: The efficacy of mesenchymal stem cell (MSC) therapy in acetaminophen-induced liver injury has been investigated in animal experiments, but individual studies with a small sample size cannot be used to draw a clear conclusion. Therefore, we conducted a systematic review and meta-analysis of preclinical studies to explore the potential of using MSCs in acetaminophen-induced liver injury. Methods: Eight databases were searched for studies reporting the effects of MSCs on acetaminophen hepatoxicity. The Preferred Reporting Items for Systematic Reviews and Meta-analyses (PRISMA) guidelines were used. SYRCLE’s risk of bias tool for animal studies was applied to assess the methodological quality. A meta-analysis was performed by using RevMan 5.4 and STATA/SE 16.0 software. Results: Eleven studies involving 159 animals were included according to PRISMA statement guidelines. Significant associations were found for MSCs with the levels of alanine transaminase (ALT) (standardized mean difference (SMD) − 2.58, p < 0.0001), aspartate aminotransferase (AST) (SMD − 1.75, p = 0.001), glutathione (GSH) (SMD 3.7, p < 0.0001), superoxide dismutase (SOD) (SMD 1.86, p = 0.022), interleukin 10 (IL-10) (SMD 5.14, p = 0.0002) and tumor necrosis factor-α (TNF-α) (SMD − 4.48, p = 0.011) compared with those in the control group. The subgroup analysis showed that the tissue source of MSCs significantly affected the therapeutic efficacy (p < 0.05). Conclusion: Our meta-analysis results demonstrate that MSCs could be a potential treatment for acetaminophen-related liver injury.

Experimental studies on the liver injury in diabetes mellitus

1967 ◽  
Vol 2 (2) ◽  
pp. 143-143
Author(s):  
J. Takeuchi ◽  
Y. Nakada ◽  
K. Ebata ◽  
G. Sawae ◽  
R. Kanayama ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Liver Injury ◽  
Experimental Studies

Experimental studies on the allergic liver injury in rats

1966 ◽  
Vol 1 (1) ◽  
pp. 52-52
Author(s):  
J. Takeuchi ◽  
T. Wakatsuki ◽  
G. Sugioka ◽  
I. Murai
Keyword(s):  
Liver Injury ◽  
Experimental Studies

scholarly journals Anti-TNF-α Treatment and Bile Duct Drainage Restore Cellular Immunity and Prevent Tissue Injury in Experimental Obstructive Jaundice

2007 ◽  
Vol 20 (4) ◽  
pp. 855-860 ◽  
Author(s):  
F.J. Padillo ◽  
A. Cruz ◽  
I. Segura-Jiménez ◽  
J. Ruiz-Rabelo ◽  
M.R. Vázquez-Ezquerra ◽  
...  
Keyword(s):  
Bile Duct ◽  
Liver Injury ◽  
Obstructive Jaundice ◽  
Renal Insufficiency ◽  
Tissue Injury ◽  
Experimental Studies ◽  
Inflammatory Cells ◽  
Activation Markers ◽  
Tnf Α ◽  
The Impact

Several experimental studies of obstructive jaundice (OJ) have shown the presence of immunosuppressive state associated with the rise of tumor necrosis factor-α (TNF-α) concentration in plasma. The present study evaluates the impact of anti-TNF-α administration or bile duct drainage on the inflammatory response, liver injury and renal insufficiency in obstructed rats. OJ was induced by the ligation of bile duct in Wistar rats. The parameters were determined at 14 and 21 days after OJ. Two additional groups of animals were treated with anti-TNF-α antibodies or submitted to bile duct drainage at 14 days, and sacrificed 21 days after OJ. Cholestasis decreased glucose, and enhanced urea, Creatinin, bilirubin and transaminases. Cholestasis increased the number of different inflammatory cells (T and B lymphocytes, and monocytes-macrophages) but reduced the expression of the corresponding cellular activation markers. This low responsiveness of the inflammatory cells was related to a decreased free radical production and phagocytic activity of cells. Anti-TNF-α and bile duct drainage reduced tissue injury, and prevented the reduction of the number and activity of T lymphocytes and phagocytic cells observed at the advanced stages of cholestasis. In conclusion, anti-TNF-α and bile duct drainage improved cell immunodeficiency, and reduced liver injury, cholestasis and renal insufficiency in experimental OJ.

Cyclosporin A in Fat Emulsion Carriers: Experimental Studies on Pharmacokinetics and Tissue Distribution

1995 ◽  
Vol 76 (2) ◽  
pp. 115-121 ◽  
Author(s):  
A. Tibell ◽  
A. Lindholm ◽  
J. Sawe ◽  
G. Chen ◽  
B. Norrlind
Keyword(s):  
Cyclosporin A ◽  
Tissue Distribution ◽  
Experimental Studies ◽  
Fat Emulsion

scholarly journals Liver apoptosis is age dependent and is reduced by activation of peroxisome proliferator-activated receptor-γ in hemorrhagic shock

2010 ◽  
Vol 298 (1) ◽  
pp. G133-G141 ◽  
Author(s):  
Basilia Zingarelli ◽  
Ranjit Chima ◽  
Michael O'Connor ◽  
Giovanna Piraino ◽  
Alvin Denenberg ◽  
...  
Keyword(s):  
Liver Injury ◽  
Hemorrhagic Shock ◽  
Molecular Mechanisms ◽  
Pediatric Trauma ◽  
Experimental Studies ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Young Rats ◽  
Arterial Blood ◽  
Age Dependent

A clinical observation in pediatric and adult intensive care units is that the incidence of multiple organ failure in pediatric trauma victims is lower than in adult patients. However, the molecular mechanisms are not yet defined. Recent experimental studies have shown that the nuclear peroxisome proliferator-activated receptor-γ (PPARγ) modulates the inflammatory process. In this study, we hypothesized that severity of liver injury may be age dependent and PPARγ activation may provide beneficial effects. Hemorrhagic shock was induced in anesthetized young (3–5 mo old) and mature male Wistar rats (11–13 mo old) by withdrawing blood to a mean arterial blood pressure of 50 mmHg. After 3 h, rats were rapidly resuscitated with shed blood. Animals were euthanized 3 h after resuscitation. In mature rats, liver injury appeared more pronounced compared with young rats and was characterized by marked hepatocyte apoptosis, extravasation of erythrocytes, and accumulation of neutrophils. The ratio between the antiapoptotic protein Bcl-2 and the proapoptotic protein BAX was lower, whereas activity of caspase-3, the executioner of apoptosis, was higher in liver of mature rats compared with young rats. Plasma alanine aminotransferase levels were not different between the two age groups. This heightened liver apoptosis was associated with a significant downregulation of PPARγ DNA binding in mature rats compared with young rats. Treatment with the PPARγ ligand ciglitazone significantly reduced liver apoptosis in mature rats. Our data suggest that liver injury after severe hemorrhage is age dependent and PPARγ activation is a novel hepatoprotective mechanism.

EXPERIMENTAL STUDIES ON TOXIC LIVER INJURY

1957 ◽  
Vol 13 (2) ◽  
pp. 102-106 ◽  
Author(s):  
H. B. STONER ◽  
P. N. MAGEE
Keyword(s):  
Liver Injury ◽  
Experimental Studies ◽  
Toxic Liver Injury

scholarly journals TNF-alpha but not IL-1alpha are Correlated with PGE1-Dependent Protection Against Acute D-Galactosamine-Induced Liver Injury

2000 ◽  
Vol 14 (3) ◽  
pp. 175-180 ◽  
Author(s):  
J Muntané ◽  
JL Montero ◽  
JM Lozano ◽  
A Miranda-Vizuete ◽  
M de la Mata ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Liver Injury ◽  
Acute Liver Injury ◽  
Experimental Studies ◽  
Acute Hepatic Failure ◽  
Inflammatory Cells ◽  
Control Group ◽  
Prostaglandin E ◽  
Necrosis Factor Alpha ◽  
Tnf Α

BACKGROUND: Prostaglandin E1(PGE1) treatment of humans and rodents during acute hepatic failure ameliorates different parameters of hepatic dysfunction.PURPOSE: To investigate whether prevention of acute liver injury induced by D-galactosamine (D-GalN) with preadministration of PGE1is correlated with a change in the concentration of two proinflammatory cytokines, as tumour necrosis factor-alpha (TNF-α) and interleukin (IL)-1α, and/or nitrite+nitrate (NOx), as nitric oxide-related end products in serum.RESULTS: D-GalN significantly increased alanine aminotransferase (ALT) and TNF- αconcentration in serum 5 and 10 mins, respectively, after treatment compared with the control group (P&#8804;0.05). D-GalN did not change the IL-1α concentration at any time during the study. Preadministration of PGE1to D-GalN-treated rats significantly reduced the ALT content and increased significantly the TNF-α concentration in serum 1, 2.5, 5 and 10 mins after D-GalN treatment compared with the D-GalN group (P&#8804;0.05). Nitric oxide was not involved in either the toxic effect due to D-GalN or the protection observed with PGE1against D-GalN toxicity.CONCLUSIONS: Acute liver injury induced by D-GalN is correlated with an increased TNF-α release. Preadministration of PGE1to D-GalN-treated rats exerted a priming effect on inflammatory cells to release enhanced levels of TNF-α but not IL-1α. These findings indicate that stimulation of TNF-α release may be involved in the acute D-GalN-induced liver injury and also in PGE1protection from hepatotoxicity in clinical and experimental studies.

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