scholarly journals Myeloid-MyD88 Contributes to Ethanol-Induced Liver Injury in Mice Linking Hepatocellular Death to Inflammation

2017 ◽  
Vol 41 (4) ◽  
pp. 719-726 ◽  
Author(s):  
Hao Zhou ◽  
Minja Yu ◽  
Sanjoy Roychowdhury ◽  
Carlos Sanz-Garcia ◽  
Katherine A. Pollard ◽  
...  
2018 ◽  
Vol 68 (5) ◽  
pp. 996-1005 ◽  
Author(s):  
Kateryna Levada ◽  
Nurdan Guldiken ◽  
Xiaoji Zhang ◽  
Giovanna Vella ◽  
Fa-Rong Mo ◽  
...  

2016 ◽  
Vol 291 (52) ◽  
pp. 26794-26805 ◽  
Author(s):  
Arvin Iracheta-Vellve ◽  
Jan Petrasek ◽  
Benedek Gyongyosi ◽  
Abhishek Satishchandran ◽  
Patrick Lowe ◽  
...  

2016 ◽  
Vol 311 (1) ◽  
pp. G156-G165 ◽  
Author(s):  
Youcai Tang ◽  
Peter Fickert ◽  
Michael Trauner ◽  
Nancy Marcus ◽  
Keith Blomenkamp ◽  
...  

The bile acid nor-ursodeoxycholic acid (norUDCA) has many biological actions, including antiapoptotic effects. Homozygous PIZZ α-1-antitrypsin (A1AT)-deficient humans are known to be at risk for liver disease, cirrhosis, and liver cancer as a result of the accumulation of the toxic, A1AT mutant Z protein within hepatocytes. This accumulation triggers cell death in the hepatocytes with the largest mutant Z-protein burdens, followed by compensatory proliferation. Proteolysis pathways within the hepatocyte, including autophagy, act to reduce the intracellular burden of A1AT Z protein. We hypothesized that norUDCA would reduce liver cell death and injury in A1AT deficiency. We treated groups of PiZ transgenic mice and wild-type mice with norUDCA or vehicle, orally, and examined the effects on the liver. The PiZ mouse is the best model of A1AT liver injury and recapitulates many features of the human liver disease. Mice treated with norUDCA demonstrated reduced hepatocellular death by compensatory hepatocellular proliferation as determined by bromodeoxyuridine incorporation (3.8% control, 0.88% treated, P < 0.04). Ki-67 staining as a marker for hepatocellular senescence and death was also reduced ( P < 0.02). Reduced apoptotic signaling was associated with norUDCA, including reduced cleavage of caspases-3, -7, and -8 (all P < 0.05). We determined that norUDCA was associated with a >70% reduction in intrahepatic mutant Z protein ( P < 0.01). A 32% increase in hepatic autophagy associated with norUDCA was the likely mechanism. norUDCA administration is associated with increased autophagy, reduced A1AT protein accumulation, and reduced liver injury in a model of A1AT deficiency.


2016 ◽  
Vol 54 (12) ◽  
pp. 1343-1404
Author(s):  
K Levada ◽  
N Guldiken ◽  
G Vella ◽  
LP James ◽  
J Haybaeck ◽  
...  

Author(s):  
F. G. Zaki

Fetal and neonatal liver injury induced by agents circulating in maternal plasma, even though well recognized, its morphological manifestations are not yet established. As part of our studies of fetal and neonatal liver injury induced by maternal nutritional disorders, metabolic impairment and toxic agents, the effects of two anti-inflammatory steroids have been recently inves tigated.Triamcinolone and methyl prednisolone were injected each in a group of rats during pregnancy at a-dosage level of 2 mgm three times a week. Fetal liver was studied at 18 days of gestation. Litter size and weight markedly decreased than those of control rats. Stillbirths and resorption were of higher incidence in the triamcinolone group than in those given the prednisolone.


2001 ◽  
Vol 120 (5) ◽  
pp. A27-A27
Author(s):  
S FLORUCCI ◽  
A MENCARELLI ◽  
B PALAZZETTI ◽  
E DISTRUTTI ◽  
G CIRINO ◽  
...  
Keyword(s):  

2001 ◽  
Vol 120 (5) ◽  
pp. A357-A357
Author(s):  
H SHIMIZU ◽  
Y FUKUDA ◽  
I NAKANO ◽  
Y KATANO ◽  
K NAGANO ◽  
...  

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