scholarly journals Hepatoprotective activity of chrysin is mediated through TNF-α in chemically-induced acute liver damage: An in vivo study and molecular modeling

2017 ◽  
Vol 13 (5) ◽  
pp. 1671-1680 ◽  
Author(s):  
Anca Hermenean ◽  
Teodora Mariasiu ◽  
Inmaculada Navarro-González ◽  
Josefina Vegara-Meseguer ◽  
Eftimie Miuțescu ◽  
...  
Keyword(s):  
Molecular Modeling ◽  
Liver Damage ◽  
Hepatoprotective Activity ◽  
In Vivo Study ◽  
Acute Liver Damage ◽  
Chemically Induced ◽  
Tnf Α

A novel fluorinated stilbene exerts hepatoprotective properties in CCl4-induced acute liver damage

2011 ◽  
Vol 89 (10) ◽  
pp. 759-766 ◽  
Author(s):  
Horacio Rivera ◽  
Martha S. Morales-Ríos ◽  
Wendy Bautista ◽  
Mineko Shibayama ◽  
Víctor Tsutsumi ◽  
...  
Keyword(s):  
Liver Damage ◽  
Inflammatory Responses ◽  
Acute Liver Damage ◽  
Tnf Α ◽  
Male Wistar Rats ◽  
Anti Inflammatory ◽  
Factor Α ◽  
Glutamyl Transpeptidase

There has been a recently increase in the development of novel stilbene-based compounds with in vitro anti-inflamatory properties. For this study, we synthesized and evaluated the anti-inflammatory properties of 2 fluorinated stilbenes on carbon tetrachloride (CCl4)-induced acute liver damage. To achieve this, CCl4 (4 g·kg–1, per os) was administered to male Wistar rats, followed by either 2-fluoro-4′-methoxystilbene (FME) or 2,3-difluoro-4′-methoxystilbene (DFME) (10 mg·kg–1, per os). We found that although both of the latter compounds prevented cholestatic damage (γ-glutamyl transpeptidase activity), only DFME showed partial but consistent results in the prevention of necrosis, as assessed by both alanine aminotransferase activity and histological analysis. Since inflammatory responses are mediated by cytokines, mainly tumour necrosis factor α (TNF-α), we used the Western blot technique to determine the action of FME and DFME on the expression level of this cytokine. The observed increase in the level of TNF-α caused by CCl4 administration was only prevented by treatment with DFME, in agreement with our biochemical findings. This result was confirmed by measuring interleukin-6 (IL-6) levels, since the expression of this protein depends on the level of TNF-α. In this case, DFME completely blocked the CCl4-induced increase of IL-6. Our results suggest that DFME possesses greater anti-inflammatory properties in vivo than FME. DFME constitutes a possible therapeutic agent for liver disease and could serve as a template for structure optimization.

scholarly journals Dipterocarpus tuberculatus Roxb. Ethanol Extract Has Anti-Inflammatory and Hepatoprotective Effects In Vitro and In Vivo by Targeting the IRAK1/AP-1 Pathway

Molecules ◽  
2021 ◽  
Vol 26 (9) ◽  
pp. 2529
Author(s):  
Haeyeop Kim ◽  
Woo Seok Yang ◽  
Khin Myo Htwe ◽  
Mi-Nam Lee ◽  
Young-Dong Kim ◽  
...  
Keyword(s):  
Ethanol Extract ◽  
Serum Levels ◽  
Hepatoprotective Activity ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Related Proteins ◽  
Pro Inflammatory Cytokines ◽  
Inflammatory Effect

Dipterocarpus tuberculatus Roxb. has been used traditionally as a remedy for many diseases, especially inflammation. Therefore, we analyzed and explored the mechanism of the anti-inflammatory effect of a Dipterocarpus tuberculatus Roxb. ethanol extract (Dt-EE). Dt-EE clearly and dose-dependently inhibited the expression of pro-inflammatory cytokines such as IL-6, TNF-α, and IL-1β in lipopolysaccharide (LPS)-treated RAW264.7 cells. Also, Dt-EE suppressed the activation of the MyD88/TRIF-mediated AP-1 pathway and the AP-1 pathway related proteins JNK2, MKK4/7, and TAK1, which occurred as a result of inhibiting the kinase activity of IRAK1 and IRAK4, the most upstream factors of the AP-1 pathway. Finally, Dt-EE displayed hepatoprotective activity in a mouse model of hepatitis induced with LPS/D-galactosamine (D-GalN) through decreasing the serum levels of alanine aminotransferase and suppressing the activation of JNK and IRAK1. Therefore, our results strongly suggest that Dt-EE could be a candidate anti-inflammatory herbal medicine with IRAK1/AP-1 inhibitory and hepatoprotective properties.

scholarly journals Metabolic Profiling of Buddleia indica Leaves using LC/MS and Evidence of their Antioxidant and Hepatoprotective Activity Using Different In Vitro and In Vivo Experimental Models

Antioxidants ◽  
2019 ◽  
Vol 8 (9) ◽  
pp. 412
Author(s):  
Fadia S. Youssef ◽  
Mohamed L. Ashour ◽  
Hesham A. El-Beshbishy ◽  
Abdel Nasser B. Singab ◽  
Michael Wink
Keyword(s):  
Antioxidant Properties ◽  
Lipid Peroxide ◽  
Hepatoprotective Activity ◽  
Experimental Models ◽  
Ionization Mass ◽  
Necrosis Factor Alpha ◽  
Stress Markers ◽  
Tnf Α

LC-ESI-MS (Liquid Chromatography coupled with Electrospray Ionization Mass Spectrometry profiling of a methanol extract from Buddleia indica (BIM) leaves revealed 12 main peaks in which verbascoside and buddlenoid B represent the major compounds. The antioxidant and hepatoprotective activities of BIM were investigated using different in vitro and in vivo experimental models. BIM exhibited substantial in vitro antioxidant properties in DPPH· and HepG2 assays. Regarding CCl4 (carbon tetrachloride) induced hepatotoxicity in a rat model, oxidative stress markers became significantly ameliorated after oral administration of BIM. Lipid peroxide levels showed a 51.85% decline relative to CCl4-treated rats. Super oxide dismutase (SOD), total antioxidant status (TAS), and catalase (CAT) revealed a marked increase by 132.48%, 187.18%, and 114.94% relative to the CCl4 group. In a tamoxifen-induced hepatotoxicity model, BIM showed a considerable alleviation in liver stress markers manifested by a 46.06% and 40% decline in ALT (Alanine Transaminase) and AST (Aspartate Transaminase) respectively. Thiobarbituric acid reactive substances (TBARS) were reduced by 28.57% and the tumor necrosis factor alpha (TNF-α) level by 50%. A virtual screening of major secondary metabolites of BIM to TNF-alpha employing the C-docker protocol showed that gmelinoside H caused the most potent TNF- α inhibition as indicated from their high fitting scores. Thus, BIM exhibited a potent hepatoprotective activity owing to its richness in antioxidant metabolites.

scholarly journals A Novel Lactic Acid Bacteria Mixture: Macrophage-Targeted Prophylactic Intervention in Colorectal Cancer Management

2020 ◽  
Vol 8 (3) ◽  
pp. 387
Author(s):  
Petra Hradicka ◽  
Jane Beal ◽  
Monika Kassayova ◽  
Andrew Foey ◽  
Vlasta Demeckova
Keyword(s):  
Colorectal Cancer ◽  
Male Rats ◽  
Cancer Management ◽  
Immune Parameters ◽  
Chemically Induced ◽  
Tnf Α ◽  
Vitro Model ◽  
Macrophage Subsets

Colorectal cancer (CRC) is one of the most common forms of cancer. Its onset from chronic inflammation is widely accepted. Moreover, dysbiosis plays an undeniable role, thus the use of probiotics in CRC has been suggested. They exhibit both anti- and pro-inflammatory properties and restore balance in the microbiota. The aim of this study was to investigate the immunomodulatory properties of six lactobacilli with probiotic features in an in vitro model of macrophage-like cells and to test these pooled probiotics for their anti-tumour properties in a chemically induced CRC model using Wistar male rats. Upon co-culture of M1- and M2-like macrophages with lactobacilli, cytokine release (TNF-α, IL-1β, IL-18, IL-23) and phagocytic activity using fluorescent-labelled bacteria were tested. The effects of orally administered probiotics on basic cancer and immune parameters and cytokine concentration (TNF-α, IL-1β, IL-18) in colon tumours were studied. Tested lactobacilli exhibited both pro- and anti-inflammatory properties in in vitro conditions. In vivo study showed that the administration of probiotics was able to decrease multiplicity, volume and total tumour numbers, restore colon length (p < 0.05) and increase IL-18 production (p < 0.05) in tumour tissue. These data indicate both an immunomodulatory effect of probiotics on distinct macrophage subsets and a protective effect against chemically-induced CRC.

An In Vitro and In Vivo Study on the Intensity of Adhesion and Colonization by Staphylococcus epidermidis and Pseudomonas aeruginosa on Originally Synthesized Biomaterials With Different Chemical Composition and Modified Surfaces and Their Effect on Expression of TNF-α, β-Defensin 2 and IL-10 in Tissues

Medicina ◽  
2011 ◽  
Vol 47 (10) ◽  
pp. 80 ◽  
Author(s):  
Aigars Reinis ◽  
Māra Pilmane ◽  
Agnese Stunda ◽  
Jānis Vētra ◽  
Juta Kroiča ◽  
...  
Keyword(s):  
Bacterial Adhesion ◽  
Bacterial Colonization ◽  
Cell Activity ◽  
In Vivo Study ◽  
Plate Count ◽  
Nonspecific Resistance ◽  
Colony Forming Units ◽  
Tnf Α

The aim of this study was to determine adhesion and colonization of bacteria on the surface of originally synthesized glass-ceramic biomaterials and their effect on inflammation reactions in tissues surrounding the implant. Materials and Methods. Biomaterial discs were contaminated with bacterial suspensions of 10, 102, and 103 colony forming units (CFU)/mL (P. aeruginosa ATCC 27853 and S. epidermidis ATCC 12228), and after 2 hours of cultivation, the intensity of bacterial adhesion was determined. For in vivo tests, the samples were contaminated with 102 and 103 CFU/mL cultivated at 37oC for 2 h to ensure bacterial adhesion. Contaminated biomaterial samples were implanted in the interscapular area of chinchilla rabbits for 2 and 4 weeks. The biomaterials were removed, and using plate count and sonification methods, bacterial colonization on the surface of biomaterials was determined. Moreover, the expression of TNF-α, β-defensin 2, and IL-10 in the surrounding tissues was assessed by using immunohistochemistry methods. Results. P. aeruginosa more intensively colonized biomaterials in the in vivo study as compared with S. epidermidis. Il-10 is a regulatory cytokine, which reduces the intensity of inflammatory cell activity, thus reducing nonspecific resistance of the organism. Conclusions. The expression of TNF-α and IL-10 was not affected by short (2 and 4 weeks) biomaterial implantation. Pronounced cytokine expression in tissues around implanted biomaterials contaminated with P. aeruginosa was observed.

scholarly journals Hepatoprotective Activity of the Total Saponins fromActinidia valvataDunn Root against Carbon Tetrachloride-Induced Liver Damage in Mice

2012 ◽  
Vol 2012 ◽  
pp. 1-13 ◽  
Author(s):  
Liping Qu ◽  
Hailiang Xin ◽  
Guoyin Zheng ◽  
Yonghua Su ◽  
Changquan Ling
Keyword(s):  
Carbon Tetrachloride ◽  
Liver Damage ◽  
Caspase 3 ◽  
Hepatoprotective Activity ◽  
Serum Marker ◽  
Acute Liver Damage ◽  
Inflammatory Infiltration ◽  
Liver Histopathology ◽  
Protein Expressions

The protective activity of the total saponins fromActinidia valvataDunn root (TSAV) was studied against carbon-tetrachloride- (CCl4-) induced acute liver injury in mice. Mice were orally administered TSAV (50, 100, and 200 mg/kg) for five days and then given CCl4. TSAV pretreatment significantly prevented the CCl4-induced hepatic damage as indicated by the serum marker enzymes (AST, ALT, and ALP). Parallel to these changes, TSAV also prevented CCl4-induced oxidative stress by inhibiting lipid peroxidation (MDA) and restoring the levels of antioxidant enzymes (SOD, CAT, GR, and GPX), GSH and GSSG. In addition, TSAV attenuated the serum TNF-αand IL-6 levels and inhibited the serum iNOS and NO levels. Liver histopathology indicated that TSAV alleviated CCl4-induced inflammatory infiltration and focal necrosis. TSAV (200 mg/kg) also significantly decreased Bak, Bax mRNA and Fas, FasL, p53, and NF-κB p65 protein expressions and increased Bcl-2 mRNA and protein expressions. Meanwhile, TSAV significantly downregulated caspase-3 and caspase-8 activities and prevented CCl4-induced hepatic cell apoptosis. In addition, TSAV exhibited antioxidant activity through scavenging hydroxyl and DPPH free radicalsin vitro. These results indicated that TSAV could protect mice against CCl4-induced acute liver damage possibly through antioxidant, anti-inflammatory activities and regulating apoptotic-related genes.

Stellate cell specific overexpression of IGF-I reduces acute liver damage induced by carbon-tetrachloride in vivo

2000 ◽  
Vol 118 (4) ◽  
pp. A1013
Author(s):  
Song Ling Liu ◽  
Sonia Sanz ◽  
Jolanta B. Pucilowska ◽  
C. Randall Fuller ◽  
Jesus Prieto ◽  
...  
Keyword(s):  
Carbon Tetrachloride ◽  
Liver Damage ◽  
Stellate Cell ◽  
Acute Liver Damage ◽  
Igf I

scholarly journals Isolation and in vivo hepatoprotective activity of Melothria heterophylla (Lour.) Cogn. against chemically induced liver injuries in rats

2011 ◽  
Vol 4 (8) ◽  
pp. 619-623 ◽  
Author(s):  
Arijit Mondal ◽  
Tapan Kumar Maity ◽  
Dilipkumar Pal ◽  
Santanu Sannigrahi ◽  
Jagadish Singh
Keyword(s):  
Hepatoprotective Activity ◽  
Chemically Induced ◽  
Liver Injuries

The Protective Effect of Kirenol in Osteoarthritis: an in Vitro and in Vivo Study

2022 ◽  
Author(s):  
Wei Hu ◽  
Chao Mao ◽  
Weibin Sheng
Keyword(s):  
Cartilage Degradation ◽  
Cartilage Destruction ◽  
In Vivo Study ◽  
Griess Reaction ◽  
Tnf Α ◽  
Collagen Ii ◽  
Cox 2 ◽  
Product Compound

Abstract Background: Osteoarthritis (OA) is a chronic degenerative disease, its main characteristic involves articular cartilage destruction and inflammation response, absent of effective medical treatment. Our current research aimed to explore anti-inflammatory effect of kirenol, a diterpenoid natural product compound, in the development of OA and its potential molecular mechanism through in vitro and in vivo study.Methods: In vitro, chondrocytes were pretreated with kirenol for 2 h before IL-1β stimulation. Production of NO, PGE2, TNF-α, IL-6, aggrecan, collagen-II, MMP13and ADAMTS5 were evaluated by the Griess reaction and ELISAs. The mRNA (aggrecan and collagen-II) and protein expression (COX-2, iNOS, P65, IκB, PI3K, AKT) were measured by qRT-PCR and Western blot respectively. Immunofluorescence was used to assess the expression of collagen-II and P65. The in vivo effect of kirenol was evaluated in mice OA models induced by destabilization of the medial meniscus (DMM).Results: We found that kirenol inhibited IL-1β-induced expression of NO, PGE2, TNF-α, IL-6, COX-2, iNOS, ADAMTS-5. Besides, kirenol remarkably decreased IL-1β-induced degradation of aggrecan and collagen-II. Furthermore, kirenol significantly inhibited IL-1β-induced phosphorylation of PI3K/Akt and NF-κB signaling. In vivo, the cartilage in kirenol-treated mice exhibited less cartilage degradation and lower OARSI scores.Conclusions: Taken together, the results of this study provide potent evidence that kirenol could be utilized as a potentially therapeutic agent in prevention and treatment of OA.

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