Lactobacillus fermentum KP-3-fermented ginseng ameliorates alcohol-induced liver disease in C57BL/6N mice through the AMPK and MAPK pathways

2020 ◽  
Vol 11 (11) ◽  
pp. 9801-9809
Author(s):  
Ying You ◽  
Yan-long Liu ◽  
Zhi-Yi Ai ◽  
Yu-Shan Wang ◽  
Jun-Mei Liu ◽  
...  
Keyword(s):  
Liver Disease ◽  
Lactobacillus Fermentum ◽  
Mapk Pathways ◽  
Fermented Ginseng

L. fermentum KP-3-fermented ginseng ameliorates ALD in mice through the AMPK and MAPK pathways.

scholarly journals Alcoholic Liver Disease: A Mouse Model Reveals Protection by Lactobacillus fermentum

2016 ◽  
Vol 7 (1) ◽  
pp. e138 ◽  
Author(s):  
Rosario Barone ◽  
Francesca Rappa ◽  
Filippo Macaluso ◽  
Celeste Caruso Bavisotto ◽  
Claudia Sangiorgi ◽  
...  
Keyword(s):  
Liver Disease ◽  
Mouse Model ◽  
Alcoholic Liver Disease ◽  
Lactobacillus Fermentum

Lactobacillus fermentum CQPC06 in naturally fermented pickles prevents non-alcoholic fatty liver disease by stabilizing the gut–liver axis in mice

2020 ◽  
Vol 11 (10) ◽  
pp. 8707-8723
Author(s):  
Jianfei Mu ◽  
Fang Tan ◽  
Xianrong Zhou ◽  
Xin Zhao
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Regulatory Mechanism ◽  
Lactobacillus Fermentum ◽  
Preventive Effect ◽  
Alcoholic Fatty Liver ◽  
Alcoholic Fatty Liver Disease

Herein, we used a HFD/F to induce NAFLD in mice and intervened with CQPC06 to determine the preventive effect of CQPC06 on NAFLD and its potential regulatory mechanism.

Protective effects of enhanced minor ginsenosides in Lactobacillus fermentum KP-3-fermented ginseng in mice fed a high fat diet

2018 ◽  
Vol 9 (11) ◽  
pp. 6020-6028 ◽  
Author(s):  
Bo Nan ◽  
Yan-long Liu ◽  
Ying You ◽  
Wan-cong Li ◽  
Jing-jing Fan ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Lactobacillus Fermentum ◽  
Protective Effects ◽  
High Fat ◽  
Fermented Ginseng

Lactobacillus fermentum KP-3 was isolated from Korean pickle and used to ferment ginseng.

Crystalloid Inclusions in Hepatocyte Mitochondria and Their Similarity to Cytoplasmic Crystalloids

1974 ◽  
Vol 32 ◽  
pp. 198-199
Author(s):  
Odell T. Minick ◽  
Hidejiro Yokoo
Keyword(s):  
Liver Disease ◽  
Alcoholic Liver Disease ◽  
Special Interest ◽  
Structural Variations ◽  
Mitochondrial Alterations ◽  
The Matrix ◽  
Crystalloid Inclusions ◽  
Liver Biopsies

Mitochondrial alterations were studied in 25 liver biopsies from patients with alcoholic liver disease. Of special interest were the morphologic resemblance of certain fine structural variations in mitochondria and crystalloid inclusions. Four types of alterations within mitochondria were found that seemed to relate to cytoplasmic crystalloids.Type 1 alteration consisted of localized groups of cristae, usually oriented in the long direction of the organelle (Fig. 1A). In this plane they appeared serrated at the periphery with blind endings in the matrix. Other sections revealed a system of equally-spaced diagonal lines lengthwise in the mitochondrion with cristae protruding from both ends (Fig. 1B). Profiles of this inclusion were not unlike tangential cuts of a crystalloid structure frequently seen in enlarged mitochondria described below.

Healing gone wrong: convergence of hemostatic pathways and liver fibrosis?

2020 ◽  
Vol 134 (16) ◽  
pp. 2189-2201
Author(s):  
Jessica P.E. Davis ◽  
Stephen H. Caldwell
Keyword(s):  
Wound Healing ◽  
Liver Disease ◽  
Hepatic Fibrosis ◽  
Cell Activation ◽  
Stellate Cell ◽  
Factor Xa ◽  
Clinical Trial Data ◽  
Chronic Liver ◽  
Healing Response ◽  
Wound Healing Response

Abstract Fibrosis results from a disordered wound healing response within the liver with activated hepatic stellate cells laying down dense, collagen-rich extracellular matrix that eventually restricts liver hepatic synthetic function and causes increased sinusoidal resistance. The end result of progressive fibrosis, cirrhosis, is associated with significant morbidity and mortality as well as tremendous economic burden. Fibrosis can be conceptualized as an aberrant wound healing response analogous to a chronic ankle sprain that is driven by chronic liver injury commonly over decades. Two unique aspects of hepatic fibrosis – the chronic nature of insult required and the liver’s unique ability to regenerate – give an opportunity for pharmacologic intervention to stop or slow the pace of fibrosis in patients early in the course of their liver disease. Two potential biologic mechanisms link together hemostasis and fibrosis: focal parenchymal extinction and direct stellate cell activation by thrombin and Factor Xa. Available translational research further supports the role of thrombosis in fibrosis. In this review, we will summarize what is known about the convergence of hemostatic changes and hepatic fibrosis in chronic liver disease and present current preclinical and clinical data exploring the relationship between the two. We will also present clinical trial data that underscores the potential use of anticoagulant therapy as an antifibrotic factor in liver disease.

Keratin 8 mutations in patient with cryptogenic liver disease

2001 ◽  
Vol 120 (5) ◽  
pp. A45-A45
Author(s):  
N KU ◽  
R GISH ◽  
T WRIGHT ◽  
M OMARY
Keyword(s):  
Liver Disease ◽  
Keratin 8

Genetic predictors of spontaneous viral elimination or chronic liver disease in hepatitis C infection

2001 ◽  
Vol 120 (5) ◽  
pp. A7-A7
Author(s):  
S ROSS ◽  
S MASCHERETTI ◽  
H HINRICHSEN ◽  
P BUGGISCH ◽  
U FOELSCH ◽  
...  
Keyword(s):  
Liver Disease ◽  
Hepatitis C ◽  
Chronic Liver Disease ◽  
Chronic Liver ◽  
Hepatitis C Infection ◽  
Genetic Predictors
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