scholarly journals Hepatoprotective Effects of Morchella esculenta against Alcohol-Induced Acute Liver Injury in the C57BL/6 Mouse Related to Nrf-2 and NF-κB Signaling

2019 ◽  
Vol 2019 ◽  
pp. 1-12
Author(s):  
Bo Meng ◽  
Yuanzhu Zhang ◽  
Zhuqian Wang ◽  
Qinran Ding ◽  
Jia Song ◽  
...  
Keyword(s):  
Superoxide Dismutase ◽  
Liver Injury ◽  
Heme Oxygenase ◽  
Liver Tissue ◽  
Nuclear Factor Kappa B ◽  
Acute Liver Injury ◽  
Nuclear Factor ◽  
Nuclear Factor Kappa ◽  
Morchella Esculenta ◽  
Hepatoprotective Effects

This study investigated the hepatoprotective effects of Morchella esculenta fruit body (ME) and the underlying mechanisms in mice with alcohol-induced acute liver injury. Systematic analysis revealed that ME contained 21 types of fatty acid, 17 types of amino acid, and 12 types of mineral. Subsequently, a mouse model of acute alcohol-induced liver injury was established by oral administration of alcohol for 14 days. Fourteen-day administration of ME prevented alcohol-induced increases in alanine aminotransferase and aspartate aminotransferase levels and reduced the activity of acetaldehyde dehydrogenase in blood serum and liver tissue. ME appears to regulate lipid metabolism by suppressing triglycerides, total cholesterol, and high-density lipoprotein in the liver. ME inhibited the production of inflammatory factors including chitinase-3-like protein 1 (YKL 40), interleukin-7 (IL-7), plasminogen activator inhibitor type 1 (PAI-1), and retinol-binding protein 4 (RBP4) in blood serum and/or liver tissue. ME treatment relieved the alcohol-induced imbalance in prooxidative and antioxidative signaling via nuclear factor-erythroid 2-related factor 2 (Nrf-2), as indicated by upregulation of superoxide dismutase-1, superoxide dismutase-2, catalase, heme oxygenase-1, and heme oxygenase-2 expression and downregulation of kelch-like ECH-associated protein 1 (Keap-1) in the liver. Moreover, ME reduced the levels of phosphorylated nuclear factor kappa-B kinase α/β, inhibitor of nuclear factor kappa-B α and nuclear factor kappa-B p65 (NF-κB p65) in the liver. The hepatoprotective effects of ME against alcohol-induced acute liver injury were thus confirmed. The mechanism of action may be related to modulation of antioxidative and anti-inflammatory signaling pathways, partially via regulation of Nrf-2 and NF-κB signaling.

Anti-Inflammatory and Hepatoprotective Effects of Ganoderma lucidum Polysaccharides against Carbon Tetrachloride-Induced Liver Injury in Kunming Mice

Pharmacology ◽  
2019 ◽  
Vol 103 (3-4) ◽  
pp. 143-150 ◽  
Author(s):  
Yu-Sheng Chen ◽  
Quan-Zhan Chen ◽  
Zhen-Jiong Wang ◽  
Chun Hua
Keyword(s):  
Carbon Tetrachloride ◽  
Liver Injury ◽  
Liver Tissue ◽  
Ganoderma Lucidum ◽  
Acute Liver Injury ◽  
Liver Weight ◽  
Inflammatory Factors ◽  
Ganoderma Lucidum Polysaccharides ◽  
Hepatoprotective Effects ◽  
Anti Inflammatory

Background: Ganoderma lucidum Polysaccharides (GLPS) were found to possess various pharmacological properties including anti-inflammatory and hepatoprotective activities. However, the effect and possible mechanism of GLPS treatment on liver injury have not yet been reported. Therefore, this study aimed to explore the potential anti-inflammatory and hepatoprotective effects and possible mechanism of GLPS in carbon tetrachloride (CCl4)-induced acute liver injury mice. Summary: GLPS significantly reduced the activation of NLRP3 inflammasome and improved liver function in liver injury mice. It significantly inhibited CCl4-induced changes of alanine aminotransferase and aspartate aminotransferase activities in serum, as well as nitric oxide synthase (NOS) and cytochrome P450 2E1 (CYP2E1) activities in liver tissue; it also remarkably decreased levels of liver weight and index, total bilirubin, interleukin (IL)-1β, IL-18, IL-6 and tumor necrosis factor-α in serum, as well as malondialdehyde and IL-1β in liver tissue. Protein expression levels of liver NLRP3, ASC, and Caspase-1 were also downregulated, while the glutathione level in liver tissue was remarkably enhanced in GLPS groups compared to that of the model group. Key Message: These results suggested that GLPS may be a potential for the prevention and treatment of acute liver injury with liver inflammation. The possible mechanism may be related to the inhibition of free radical lipid peroxidation, NOS, and CYP2E1 activities and activation of liver inflammatory factors.

scholarly journals KCHO-1, a Novel Antineuroinflammatory Agent, Inhibits Lipopolysaccharide-Induced Neuroinflammatory Responses through Nrf2-Mediated Heme Oxygenase-1 Expression in Mouse BV2 Microglia Cells

2014 ◽  
Vol 2014 ◽  
pp. 1-11 ◽  
Author(s):  
Dong-Sung Lee ◽  
Wonmin Ko ◽  
Chi-Su Yoon ◽  
Dong-Cheol Kim ◽  
Jinju Yun ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Neurodegenerative Diseases ◽  
Heme Oxygenase ◽  
Nuclear Factor Kappa B ◽  
Heme Oxygenase 1 ◽  
Related Factor ◽  
Nuclear Factor ◽  
Nuclear Factor Kappa ◽  
Bv2 Microglia ◽  
Cox 2

The brain is vulnerable to oxidative stress and inflammation that can occur as a result of aging or neurodegenerative diseases. Our work has sought to identify natural products that regulate heme oxygenase (HO)-1 and to determine their mechanism of action in neurodegenerative diseases. KCHO-1 is a novel herbal therapeutic containing 30% ethanol (EtOH) extracts from nine plants. In this study, we investigated the antineuroinflammatory effects of KCHO-1 in lipopolysaccharide- (LPS-) treated mouse BV2 microglia. KCHO-1 inhibited the protein expression of inducible nitric oxide synthase (iNOS), iNOS-derived nitric oxide (NO), cyclooxygenase- (COX-) 2, and COX-2-derived prostaglandin E2 (PGE2) in LPS-stimulated BV2 microglia. It also reduced tumor necrosis factor-α(TNF-α), interleukin-1β(IL-1β), and IL-6 production. This effect was correlated with the suppression of inhibitor of nuclear factor kappa B-α(IκB-α) phosphorylation and degradation and nuclear factor kappa B (NF-κB) translocation and DNA binding. Additionally, KCHO-1 upregulated HO-1 expression by promoting nuclear translocation of nuclear factor E2-related factor 2 (Nrf2) in mouse BV2 microglia. Tin protoporphyrin (SnPP), an HO activity inhibitor, was used to verify the inhibitory effects of KCHO-1 on proinflammatory mediators and proteins associated with HO-1 expression. Our data suggest that KCHO-1 has therapeutic potential in neurodegenerative diseases caused by neuroinflammation.

Dietary glycine inhibits activation of nuclear factor kappa B and prevents liver injury in hemorrhagic shock in the rat

2001 ◽  
Vol 31 (10) ◽  
pp. 1236-1244 ◽  
Author(s):  
J.L Mauriz ◽  
B Matilla ◽  
J.M Culebras ◽  
P González ◽  
J González-Gallego
Keyword(s):  
Liver Injury ◽  
Hemorrhagic Shock ◽  
Nuclear Factor Kappa B ◽  
Nuclear Factor ◽  
Nuclear Factor Kappa

Sanguinarine Ameliorates Diabetic Nephropathy in Rats through Nuclear Factor-Kappa B and Nuclear-Factor Erythroid 2-Related Factor 2/Heme Oxygenase-1 Pathways

2021 ◽  
Vol 19 (4) ◽  
pp. 398-404
Author(s):  
Jiao Zhong
Keyword(s):  
Diabetic Nephropathy ◽  
Heme Oxygenase ◽  
Nuclear Factor Kappa B ◽  
Kidney Injury ◽  
Diabetic Rats ◽  
Heme Oxygenase 1 ◽  
Related Factor ◽  
Nuclear Factor ◽  
Related Complication ◽  
Nuclear Factor Kappa

Alkaloids - derived from natural plants - were widely used for therapy in diabetes or diabetes-related complications. Sanguinarine, a benzophenanthridine alkaloid derived from Sanguinaria canadensis, has been identified as a potential drug for type 2 diabetes. However, the role of sanguinarine on diabetes-related complication, diabetic nephropathy, has not been reported yet. In a rat model of diabetic nephropathy we have demonstrated increased levels of 24 h urinary proteins, serum creatinine, and blood urea nitrogen, as well as series of degenerative changes in the kidney tissues. Oral administration with sanguinarine to diabetic rats diminished kidney injury markers and improved the tissue morphology. Furthermore, sanguinarine attenuated increase in the levels of tumor necrosis factor-α and interleukin-6 through downregulation of phosphonuclear factor-kappa B and phosphorylated inhibitor of nuclear factor kappa-B. Lastly, sanguinarine reversed the effects of streptozotocin on levels of reactive oxygen species, malonaldehyde, superoxide dismutase, and glutathione peroxidase through upregulation of nuclear factor erythropoietin-2-related factor 2, heme oxygenase 1 and NAD(P)H quinone dehydrogenase 1 in kidney of rats. In conclusion, sanguinarine ameliorates diabetic nephropathy in rats through inactivation of nuclear factor-kappa B and activation of nuclear-factor erythroid 2-related factor 2 pathways.

Dihydroresveratrol Improves Liver Injury in Septic Rats by Regulating Nuclear Factor-Kappa B Signaling Pathway

2021 ◽  
Vol 20 (1) ◽  
pp. 37-42
Author(s):  
Jinjing Hong ◽  
Jinchao Mao ◽  
Zhitao Zeng ◽  
Chunlian Ma ◽  
Miaoyao Lin ◽  
...  
Keyword(s):  
Liver Injury ◽  
Signaling Pathway ◽  
Inflammatory Process ◽  
Nuclear Factor Kappa B ◽  
Parasitic Infections ◽  
Nuclear Factor ◽  
Antitumor Effects ◽  
Nuclear Factor Kappa ◽  
Novel Drugs

Sepsis is a severe systemic inflammatory response syndrome caused by bacterial, fungal, viral, or parasitic infections. During sepsis, proinflammatory cytokines play a key role in initiating the inflammatory process. It is still urgently needed to develop novel drugs for sepsis treatment. Dihydroresveratrol is a polyphenol derivative belonging to phenylpropane, which has anti-inflammatory, antifibrosis, antiaging, and antitumor effects, whereas the role of dihydroresveratrol in sepsis is still unclear. In this study, we observed that dihydroresveratrol improved septic liver injury. We further observed that dihydroresveratrol decreased the expression of inflammatory cytokines and oxidative damage to rat liver tissues. Dihydroresveratrol improved liver injury in septic rats via regulating nuclear factor-kappa B signaling pathway.

scholarly journals Hepatoprotective Effects of Antrodia cinnamomea: The Modulation of Oxidative Stress Signaling in a Mouse Model of Alcohol-Induced Acute Liver Injury

2017 ◽  
Vol 2017 ◽  
pp. 1-12 ◽  
Author(s):  
Yange Liu ◽  
Juan Wang ◽  
Lanzhou Li ◽  
Wenji Hu ◽  
Yidi Qu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Injury ◽  
Mouse Model ◽  
Caspase 3 ◽  
Acute Liver Injury ◽  
Nuclear Factor ◽  
Related Factors ◽  
Inflammatory Infiltration ◽  
Hepatoprotective Effects ◽  
Underlying Mechanisms

In the present study, the components of A. cinnamomea (AC) mycelia were systematically analyzed. Subsequently, its hepatoprotective effects and the underlying mechanisms were explored using a mouse model of acute alcohol-induced liver injury. AC contained 25 types of fatty acid, 16 types of amino acid, 3 types of nucleotide, and 8 types of mineral. The hepatoprotective effects were observed after 2 weeks of AC treatment at doses of 75 mg/kg, 225 mg/kg, and 675 mg/kg in the mouse model. These effects were indicated by the changes in the levels of aspartate aminotransferase, alanine aminotransferase, several oxidation-related factors, and inflammatory cytokines in serum and/or liver samples. AC reduced the incidence rate of necrosis, inflammatory infiltration, fatty droplets formation, and cell apoptosis in liver detecting via histological and TUNEL assay. In addition, AC reduced the expression of cleaved caspase-3, -8, and -9 and the levels of phosphor-protein kinase B (Akt) and phosphor-nuclear factor-κB (NF-κB) in the liver samples. Collectively, AC-mediated hepatoprotective effects in a mouse model of acute alcohol-induced liver injury are the result of reduction in oxidative stress. This may be associated with Akt/NF-κB signaling. These results provide valuable evidence to support the use of A. cinnamomea as a functional food and/or medicine.

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