scholarly journals Serum Autotaxin is a Marker of the Severity of Liver Injury and Overall Survival in Patients with Cholestatic Liver Diseases

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Ewa Wunsch ◽  
Marcin Krawczyk ◽  
Malgorzata Milkiewicz ◽  
Jocelyn Trottier ◽  
Olivier Barbier ◽  
...  
Keyword(s):  
Overall Survival ◽  
Liver Injury ◽  
Liver Diseases

A polysaccharide of PFP-1 from Pleurotus geesteranus attenuates alcoholic liver diseases via Nrf2 and NF-κB signaling pathways

2021 ◽  
Author(s):  
Xinling Song ◽  
Wenxue Sun ◽  
Wenxin Cai ◽  
Le Jia ◽  
Jianjun Zhang
Keyword(s):  
Oxidative Stress ◽  
Liver Disease ◽  
Liver Injury ◽  
Signaling Pathways ◽  
Alcoholic Liver Disease ◽  
Fruiting Body ◽  
Liver Diseases ◽  
Alcoholic Liver Diseases

A polysaccharide named as PFP-1 was isolated from Pleurotus geesteranus fruiting body, and the potential investigations on ameliorating oxidative stress and liver injury against alcoholic liver disease (ALD) were processed...

Enhancing therapeutic effects and in vivo tracking of adipose tissue derived mesenchymal stem cells for liver injury using bioorthogonal click chemistry

Nanoscale ◽  
2020 ◽  
Author(s):  
Naishun Liao ◽  
Da Zhang ◽  
Ming Wu ◽  
Huang-Hao Yang ◽  
Xiaolong Liu ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Adipose Tissue ◽  
Stem Cell ◽  
Liver Injury ◽  
Mesenchymal Stem Cell ◽  
Liver Diseases ◽  
Therapeutic Effects

Adipose tissue derived mesenchymal stem cell (ADSC)-based therapy is attractive for liver diseases, but the long-term therapeutic outcome is still far from satisfaction due to low hepatic engraftment efficiency of...

Hepatology after Hepatitis C

2016 ◽  
Vol 34 (5) ◽  
pp. 603-606 ◽  
Author(s):  
J. Gregory Fitz
Keyword(s):  
Liver Disease ◽  
Hepatitis C ◽  
Liver Injury ◽  
Early Detection ◽  
Liver Diseases ◽  
Population Level ◽  
Success Stories ◽  
Risk Variants ◽  
Complications Of Cirrhosis ◽  
Direct Acting

The ∼90% probability of curing individual patients with hepatitis C virus (HCV)using direct-acting antivirals represents one of the most dramatic medical success stories of the modern era, and the journey from viral discovery to treatment occurred over just ∼25 years. The realities of the global burden of disease (2-3% of the world's population is infected), limited access to care and cost of treatment mean that HCV will continue to be a major problem for the next 25 years. But what if HCV (and hepatitis B) could be eradicated? Since liver transplantation and HCV management have been the mainstays of academic hepatology practice, where do we go from here? Unfortunately, we are in an era where the incidence and prevalence of liver diseases around the globe is increasing, and death from complications of cirrhosis is now among the top 10 causes in most countries; so hepatologists are expected to play a major role in the future. Despite remarkable progress, success at the population level is limited by the resource-intensive nature of caring for patients with end-stage disease. Accordingly, the major advances in the next decade are likely to focus on (i) the earlier identification of individuals and populations at higher risk for liver diseases, and (ii) initiation in high-risk populations of specific strategies for early detection and treatment of fibrosis, cancer and cirrhosis. The answers will lie in large part in the further exploration of the human genome in carefully phenotyped patients. Risk variants in the PNPLA3 gene represent the best example to date. The risk variants are common and are enriched in certain populations around the globe; and individuals that possess risk variants are more likely to have liver injury from fatty liver disease (even as children), alcohol and viral hepatitis. Further, those with liver injury are more likely to progress to cirrhosis and hepatoma. Similarly, in those with established liver disease, use of biomarkers and other strategies for early detection of fibrosis and hepatoma will pay dividends as the next generation of treatments focusing on (i) anti-fibrotic strategies and (ii) liver regeneration move to the forefront. There remains an important need to invest in hepatology as a growth industry even after the (unlikely) eradication of HCV.

Green tea polyphenols prevent lipopolysaccharide-induced inflammatory liver injury in mice by inhibiting NLRP3 inflammasome activation

2019 ◽  
Vol 10 (7) ◽  
pp. 3898-3908 ◽  
Author(s):  
Dongxu Wang ◽  
Man Zhang ◽  
Taotao Wang ◽  
Min Cai ◽  
Frank Qian ◽  
...  
Keyword(s):  
Public Health ◽  
Liver Injury ◽  
Green Tea ◽  
Liver Diseases ◽  
Public Health Problem ◽  
Green Tea Polyphenols ◽  
Inflammasome Activation ◽  
Nlrp3 Inflammasome Activation ◽  
Significant Public Health Problem ◽  
Significant Public Health

Inflammatory liver diseases present a significant public health problem.

Epimedium koreanum Ameliorates Oxidative Stress-Mediated Liver Injury by Activating Nuclear Factor Erythroid 2-Related Factor 2

2018 ◽  
Vol 46 (02) ◽  
pp. 469-488 ◽  
Author(s):  
Ji Yun Jung ◽  
Sang Mi Park ◽  
Hae Li Ko ◽  
Jong Rok Lee ◽  
Chung A Park ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Injury ◽  
Hepg2 Cells ◽  
Liver Diseases ◽  
Caspase 3 ◽  
Glutathione Depletion ◽  
Related Factor ◽  
Nuclear Factor ◽  
Nrf2 Activation ◽  
Anti Oxidant

Oxidative stress induced by reactive oxygen species is the main cause of various liver diseases. This study investigated the hepatoprotective effect of Epimedium koreanum Nakai water extract (EKE) against arachidonic acid (AA)[Formula: see text][Formula: see text][Formula: see text]iron-mediated cytotoxicity in HepG2 cells and carbon tetrachloride (CCl4-)-mediated acute liver injury in mice. Pretreatment with EKE (30 and 100[Formula: see text][Formula: see text]g/mL) significantly inhibited AA[Formula: see text][Formula: see text][Formula: see text]iron-mediated cytotoxicity in HepG2 cells by preventing changes in the expression of cleaved caspase-3 and poly(ADP-ribose) polymerase. EKE attenuated hydrogen peroxide production, glutathione depletion, and mitochondrial membrane dysfunction. EKE also increased the nuclear translocation of nuclear factor erythroid 2-related factor 2 (Nrf2), transactivated anti-oxidant response element harboring luciferase activity, and induced the expression of anti-oxidant genes. Furthermore, the cytoprotective effect of EKE against AA[Formula: see text][Formula: see text][Formula: see text]iron was blocked in Nrf2 knockout cells. Ultra-performance liquid chromatography analysis showed that EKE contained icariin, icaritin, and quercetin; icaritin and quercetin were both found to protect HepG2 cells from AA[Formula: see text][Formula: see text][Formula: see text]iron via Nrf2 activation. In a CCl4-induced mouse model of liver injury, pretreatment with EKE (300[Formula: see text]mg/kg) for four consecutive days ameliorated CCl4-mediated increases in serum aspartate aminotransferase activity, histological activity index, hepatic parenchyma degeneration, and inflammatory cell infiltration. EKE also decreased the number of nitrotyrosine-, 4-hydroxynonenal-, cleaved caspase-3-, and cleaved poly(ADP-ribose) polymerase-positive cells in hepatic tissues. These results suggest EKE is a promising candidate for the prevention or treatment of oxidative stress-related liver diseases via Nrf2 activation.

scholarly journals Towards better diagnostic tools for liver injury in low-income and middle-income countries

2019 ◽  
Vol 4 (4) ◽  
pp. e001704 ◽  
Author(s):  
Saundria Moed ◽  
Muhammad H Zaman
Keyword(s):  
Chronic Hepatitis ◽  
Liver Injury ◽  
Low Income ◽  
Liver Diseases ◽  
Diagnostic Methods ◽  
Low Income Countries ◽  
Diagnostic Tools ◽  
Middle Income ◽  
Public Health Burden ◽  
Middle Income Countries

Liver disease is a significant public health burden in both high-income and low-income countries, accounting for over 2 million annual, global deaths. Despite the significant mortality burden, liver diseases are historically a neglected problem due to a lack of accurate incidence and prevalence statistics, as well as national and international programmes targeting these diseases. A large portion of deaths due to liver diseases can be treated (eg, chronic hepatitis B), cured (eg, chronic hepatitis C) or prevented (eg, acute liver failure due to medications) if prompt diagnosis is made, but currently diagnostic methods fall short. Therefore, there is a critical need to fund the development of prompt, effective diagnostics for liver function, specifically in low-income and middle-income countries where the landscape for this testing is sparse. Here, we review and compare available and currently emerging diagnostic methods for liver injury in low-income and middle-income settings, while highlighting the opportunities and challenges that exist in the field.

Hepatoprotective Activity of Reduohanxiao-tang (Yuldahanso-tang) is Related to the Inhibition of β-Glucuronidase

2003 ◽  
Vol 31 (01) ◽  
pp. 111-117 ◽  
Author(s):  
Hyung-Sup Bae ◽  
Young-Suk Kim ◽  
Ki-Ho Cho ◽  
Kyung-Sup Lee ◽  
Jung-Jin Kim ◽  
...  
Keyword(s):  
Liver Injury ◽  
Liver Diseases ◽  
Herbal Medicines ◽  
Intestinal Bacteria ◽  
Hepatoprotective Activity ◽  
Control Group ◽  
Human Intestinal Bacteria ◽  
Serum Aspartate Aminotransferase ◽  
Hepatoprotective Effects ◽  
Main Component

β-Glucuronidase-inhibitory and hepatoprotective effects of Reduohanxiao-tang (Yuldahanso-tang), which has been used for liver diseases and stroke, on carbon tetrachloride (CCl4)-induced hepatotoxicity of rats were investigated. Reduohanxiao-tang potently inhibited β-glucuronidases. Serum aspartate aminotransferase (AST), alanine aminotransferase (ALT) and lactic acid dehydrogenase (LDH) levels of the CCl4 group orally treated with Reduohanxiao-tang (100 mg/kg) were lowered to 54%, 71.5% and 66.1% of the CCl4-treated control group, respectively. Among the ingredients of the Reduohanxiao-tang, the rhizomes of Pueraria thunbergiana and it Scutellaria baicalensis potently inhibited β-glucuronidases and protected against CCl4-induced liver injury. Orally administered puerarin, which is a main component of Pueraria thunbergiana, showed potent hepatoprotective activity, but did not inhibit β-glucuronidase. However, daidzein, which is produced from puerarin by human intestinal bacteria, potently inhibited β-glucuronidase. These results suggest that β-glucuronidase inhibition by herbal medicines may protect a gainst CCl4-induced liver injury.

scholarly journals Toll-Like Receptor 3 in Liver Diseases

2010 ◽  
Vol 2010 ◽  
pp. 1-6 ◽  
Author(s):  
Shi Yin ◽  
Bin Gao
Keyword(s):  
Liver Disease ◽  
Liver Fibrosis ◽  
Liver Injury ◽  
Immune Cells ◽  
Liver Diseases ◽  
Human Liver ◽  
Toll Like Receptor ◽  
Double Stranded Rna ◽  
Nonparenchymal Cells

Toll-like receptor 3 (TLR3) is a member of the TLR family that can recognize double-stranded RNA (dsRNA), playing an important role in antiviral immunity. Recent studies have shown that TLR3 is also expressed on parenchymal and nonparenchymal cells in the liver as well as on several types of immune cells. In this review, we summarize the role of TLR3 in liver injury, inflammation, regeneration, and liver fibrosis, and discuss the implication of TLR3 in the pathogenesis of human liver diseases including viral hepatitis and autoimmune liver disease.

Death by association: BH3 domain-only proteins and liver injury

2005 ◽  
Vol 289 (6) ◽  
pp. G987-G990 ◽  
Author(s):  
E. S. Baskin-Bey ◽  
G. J. Gores
Keyword(s):  
Cell Death ◽  
Liver Injury ◽  
Mitochondrial Dysfunction ◽  
Liver Cell ◽  
Liver Diseases ◽  
Chronic Liver Diseases ◽  
Concise Review ◽  
Bh3 Domain ◽  
A Cell

Apoptosis, a prominent form of cell death, is a prime feature of many acute and chronic liver diseases. Apoptosis requires mitochondrial dysfunction, which is regulated by proteins of the Bcl-2 family. Whether or not a cell should live or die is controlled by the interaction of multidomain Bcl-2 proteins with proapoptotic BH3 domain-only proteins of this family. Current models suggest multidomain, antiapoptotic Bcl-2 proteins prevent mitochondrial dysfunction by sequestering and/or preventing activation of its proapoptotic relatives. BH3-only proteins initiate cell death by neutralizing and or ligating multidomain prosurvival Bcl-2 proteins. Thus BH3 domain-only proteins are paramount in the apoptotic process as exemplified by the role of the BH3 domain-only protein Bid in liver injury. In this concise review, we will focus on how these BH3 domain-only proteins are regulated in the cell, their association with the Bcl-2 family of proteins, and finally, current information regarding their involvement in liver cell apoptosis and injury.

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