Treatment with milk thistle extract (Silybum marianum), ursodeoxycholic acid, or their combination attenuates cholestatic liver injury in rats: Role of the hepatic stem cells

2017 ◽  
Vol 28 (6) ◽  
pp. 476-484 ◽  
Author(s):  
Nuray Alaca ◽  
Dilek Ozbeyli ◽  
Serap Uslu ◽  
Hasan Huseyin Sahin ◽  
Gurkan Yigitturk ◽  
...  
Keyword(s):  
Stem Cells ◽  
Liver Injury ◽  
Ursodeoxycholic Acid ◽  
Milk Thistle ◽  
Hepatic Stem Cells ◽  
Silybum Marianum ◽  
Cholestatic Liver Injury

scholarly journals The Art of Mesenchymal Stem Cells in Liver Fibrosis Management

2021 ◽  
Vol 3 (2) ◽  
pp. 15-24
Author(s):  
Farid Amansyah ◽  
Dito Anurogo
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Liver Fibrosis ◽  
Liver Injury ◽  
Tissue Damage ◽  
Fundamental Concept ◽  
Scientific Review ◽  
Safety And Efficacy ◽  
Experimental Animals

Liver fibrogenesisis chronic tissue damage characterized by an extracellular ac-cumulation of fibrillar matrix associated with continuous degradation and remod-elling. This scientific review describes current concepts on the pathophysiology of liver fibrosis, inflammation asa fundamental concept of liver fibrosis, mechanistic concepts of liver fibrosis, the role of mesenchymal stem cells (MSC) in liver injury, the functional effects of MSC secretome, the advantages of secretome ther-apy, and the latest research developments on MSC. The role of MSCs has been proven in many liver fibrosis studies involving experimental animals. However, it still requires further research for safety and efficacy aspects.

scholarly journals Functional Role of the Secretin/Secretin Receptor Signaling During Cholestatic Liver Injury

Hepatology ◽  
2020 ◽  
Vol 72 (6) ◽  
pp. 2219-2227 ◽  
Author(s):  
Nan Wu ◽  
Leonardo Baiocchi ◽  
Tianhao Zhou ◽  
Lindsey Kennedy ◽  
Ludovica Ceci ◽  
...  
Keyword(s):  
Liver Injury ◽  
Functional Role ◽  
Receptor Signaling ◽  
Secretin Receptor ◽  
Cholestatic Liver Injury

scholarly journals Impact of Exogenous Application of Salicylic Acid and Hydrogen Peroxide on Essential Nutrients and Silymarin in Silybum Marianum (L.) Gaertn Grown at Two Different Altitudes of Balochistan Under Cadmium Stress

2021 ◽  
Author(s):  
Mereen Nizar ◽  
Kanval Shaukat ◽  
Noreen Zahra ◽  
Abdul Samad ◽  
Mohammad Bilal Hafeez ◽  
...  
Keyword(s):  
Hydrogen Peroxide ◽  
Salicylic Acid ◽  
Cadmium Toxicity ◽  
Foliar Spray ◽  
Cadmium Stress ◽  
Milk Thistle ◽  
Silybum Marianum ◽  
Essential Nutrients ◽  
Exogenous Application

Abstract Cadmium (Cd+2) is a potentially toxic element that inhibits growth and development of several species of plants along with Silybum marianum (L.) Gaertn which is an essential medicinal plant belonging to family Asteraceae. The exogenous application with 0.25µM Salicylic acid (SA) and 10µM hydrogen peroxide (H2O2) to ameliorate harmful effects of cadmium (500 µM) on milk thistle were studied that were grown at two different ecological zones of Balochistan province of Pakistan i.e. Quetta (Qta) and Turbat (Tbt). The design of experiment was Randomized Complete Block Design (RCBD) with three replicates. Application of SA and H2O2, priming (P), Foliar spray (FS) and combinational treatments (P+FS) were highly helpful in alleviating the negative role of cadmium toxicity. The essential nutrients i.e. nitrate (NO3-), calcium (Ca2+) and potassium (K) were affected by Cd+2 induced toxicity however, the substantial role of SA and H2O2 widely helped to reduce the cadmium stress and boosted up the plant nutrients content. In a nutshell, exogenous treatments of SA and H2O2 enhanced the yield potential along with highest silymarin contents in milk thistle seeds which is of prime significance for its medicinal importance in treatment of liver diseases. The data obtained in this study highly recommend the priming and foliar spray of SA and H2O2 on milk thistle plants, as the best solution to alleviative the cadmium toxicity which will ultimately leads to better growth and yield of the plants.

scholarly journals Loss of cellular FLICE-inhibitory protein promotes acute cholestatic liver injury and inflammation from bile duct ligation

2018 ◽  
Vol 314 (3) ◽  
pp. G319-G333 ◽  
Author(s):  
Nadine Gehrke ◽  
Michael Nagel ◽  
Beate K. Straub ◽  
Marcus A. Wörns ◽  
Marcus Schuchmann ◽  
...  
Keyword(s):  
Bile Duct ◽  
Liver Injury ◽  
Bile Acids ◽  
Bile Duct Ligation ◽  
Ex Vivo ◽  
Mapk Signaling ◽  
Caspase 8 ◽  
Duct Ligation ◽  
Cholestatic Liver Injury

Cholestatic liver injury results from impaired bile flow or metabolism and promotes hepatic inflammation and fibrogenesis. Toxic bile acids that accumulate in cholestasis induce apoptosis and contribute to early cholestatic liver injury, which is amplified by accompanying inflammation. The aim of the current study was to evaluate the role of the antiapoptotic caspase 8-homolog cellular FLICE-inhibitory (cFLIP) protein during acute cholestatic liver injury. Transgenic mice exhibiting hepatocyte-specific deletion of cFLIP (cFLIP−/−) were used for in vivo and in vitro analysis of cholestatic liver injury using bile duct ligation (BDL) and the addition of bile acids ex vivo. Loss of cFLIP in hepatocytes promoted acute cholestatic liver injury early after BDL, which was characterized by a rapid release of proinflammatory and chemotactic cytokines (TNF, IL-6, IL-1β, CCL2, CXCL1, and CXCL2), an increased presence of CD68+ macrophages and an influx of neutrophils in the liver, and resulting apoptotic and necrotic hepatocyte cell death. Mechanistically, liver injury in cFLIP−/− mice was aggravated by reactive oxygen species, and sustained activation of the JNK signaling pathway. In parallel, cytoprotective NF-κB p65, A20, and the MAPK p38 were inhibited. Increased injury in cFLIP−/− mice was accompanied by activation of hepatic stellate cells and profibrogenic regulators. The antagonistic caspase 8-homolog cFLIP is a critical regulator of acute, cholestatic liver injury. NEW & NOTEWORTHY The current paper explores the role of a classical modulator of hepatocellular apoptosis in early, cholestatic liver injury. These include activation of NF-κB and MAPK signaling, production of inflammatory cytokines, and recruitment of neutrophils in response to cholestasis. Because these signaling pathways are currently exploited in clinical trials for the treatment of nonalcoholic steatohepatitis and cirrhosis, the current data will help in the development of novel pharmacological options in these indications.

Sa1337 Treatment With Milk Thistle, Ursodeoxycholic Acid or Their Combination Attenuates Liver Injury in Bile Duct-Ligated Rats

2015 ◽  
Vol 148 (4) ◽  
pp. S-295
Author(s):  
Nuray Alaca ◽  
Dilek Ozbeyli ◽  
Serap Uslu ◽  
Hasan H. Sahin ◽  
Hizir Kurtel ◽  
...  
Keyword(s):  
Bile Duct ◽  
Liver Injury ◽  
Ursodeoxycholic Acid ◽  
Milk Thistle

scholarly journals Inflammation and Cell Death During Cholestasis: The Evolving Role of Bile Acids

2019 ◽  
Vol 19 (3) ◽  
pp. 215-228 ◽  
Author(s):  
Benjamin L. Woolbright ◽  
Hartmut Jaeschke
Keyword(s):  
Cell Death ◽  
Liver Injury ◽  
Bile Acids ◽  
Primary Role ◽  
Drug Induced ◽  
Chronic Cholestasis ◽  
Biliary Tracts ◽  
Acute Retention ◽  
Cholestatic Liver Injury

Cholestasis results in blockage of bile flow whether the point of obstruction occurs extrahepatically or intrahepatically. Bile acids are a primary constituent of bile, and thus one of the primary outcomes is acute retention of bile acids in hepatocytes. Bile acids are normally secreted into the biliary tracts and then released into the small bowel before recirculating back to the liver. Retention of bile acids has long been hypothesized to be a primary cause of the associated liver injury that occurs during acute or chronic cholestasis. Despite this, a surge of papers in the last decade have reported a primary role for inflammation in the pathophysiology of cholestatic liver injury. Furthermore, it has increasingly been recognized that both the constituency of individual bile acids that make up the greater pool, as well as their conjugation status, is intimately involved in their toxicity, and this varies between species. Finally, the role of bile acids in drug-induced cholestatic liver injury remains an area of increasing interest. The purpose of this review is to critically evaluate current proposed mechanisms of cholestatic liver injury, with a focus on the evolving role of bile acids in cell death and inflammation.

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