scholarly journals Banhasasim-Tang Treatment Reduces the Severity of Esophageal Mucosal Ulcer on Chronic Acid Reflux Esophagitis in Rats

2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
Mi-Rae Shin ◽  
Bu-Il Seo ◽  
Chang Gue Son ◽  
Seong-Soo Roh ◽  
Hyo-Jin An
Keyword(s):  
Reflux Esophagitis ◽  
Thiobarbituric Acid ◽  
Antioxidant Response ◽  
Acid Reflux ◽  
Mitogen Activated Protein Kinase ◽  
Histological Evaluation ◽  
Related Factor ◽  
Nuclear Factor ◽  
Protein Levels ◽  
Mitogen Activated Protein

The present study was conducted to evaluate both antioxidant and anti-inflammatory activity of Banhasasim-tang (BHSST) on chronic acid reflux esophagitis (CRE) model. Rat CRE model was established operatively and then treated with BHSST (1 g/kg body weight per day) for 15 days Esophageal pathological changes were analyzed using macroscopic examination and hematoxylin/eosin staining. The antioxidant and inflammatory protein levels were determined using Western blotting. The administration of BHSST significantly reduced both the overexpression of serum reactive oxygen species (ROS) and an excessive formation of thiobarbituric acid-reactive substances (TBARS) in esophagus tissue. Thus, the severity of esophageal ulcer was lower in BHSST treated rats than control rats on the gross and histological evaluation. Nuclear factor-erythroid 2-related factor 2 (Nrf2) led to the upregulation of antioxidant enzyme including SOD, GPx-1/2, and HO-1 by binding to antioxidant response element (ARE). Moreover, BHSST administration markedly reduced the expression of inflammatory proteins through mitogen-activated protein kinase- (MAPK-) related signaling pathways and decreased significantly the protein expressions of inflammatory mediators and cytokines by inhibition of nuclear factor-kappa B (NF-κB) activation. Taken together, these results support the fact that BHSST administration can suppress the development of esophageal mucosal ulcerviaregulating inflammation through the activation of the antioxidant pathway.

scholarly journals Betanin, a beetroot component, induces nuclear factor erythroid-2-related factor 2-mediated expression of detoxifying/antioxidant enzymes in human liver cell lines

2013 ◽  
Vol 110 (12) ◽  
pp. 2138-2149 ◽  
Author(s):  
Violetta Krajka-Kuźniak ◽  
Jarosław Paluszczak ◽  
Hanna Szaefer ◽  
Wanda Baer-Dubowska
Keyword(s):  
Cell Lines ◽  
Hepg2 Cells ◽  
Antioxidant Response ◽  
Related Factor ◽  
Nuclear Factor ◽  
Protein Levels ◽  
Expression Of Genes ◽  
Human Liver Cell ◽  
Mitogen Activated Protein ◽  
Hepg2 Cell Lines

Our recent study has shown that beetroot juice protects against N-nitrosodimethylamine (NDEA)-induced liver injury and increases the activity of phase II enzymes, suggesting the activation of the nuclear factor erythroid-2-related factor 2 (Nrf2)–antioxidant response element (ARE) pathway. The aim of the present study was to further explore the mechanism of the activity of beetroot by evaluating the cytoprotective effects of its major component. The influence of betanin (BET) on the activation of Nrf2 and the expression ofGSTA,GSTP,GSTM,GSTT,NQO1andHO-1was assessed in two hepatic cell lines: non-tumour THLE-2 and hepatoma-derived HepG2 cell lines. The level of the tumour suppressor p53 in both cell lines and the methylation ofGSTPin HepG2 cells were also evaluated. Treatment of both cell lines with 2, 10 and 20 μmof BET resulted in the translocation of Nrf2 from the cytosol to the nucleus. The mRNA and nuclear protein levels of Nrf2 and the binding of Nrf2 to ARE sequences were increased only in the THLE-2 cells and were accompanied by the phosphorylation of serine/threonine kinase (AKT), c-Jun N-terminal kinase (JNK) and extracellular signal-regulated kinase (ERK). BET also significantly increased the mRNA and protein levels of GSTP, GSTT, GSTM and NQO1 in these cells. Conversely, besides the translocation of Nrf2 from the cytosol to the nucleus, BET did not modulate any of the other parameters measured in the HepG2 cells. BET did not change the methylation ofGSTP1in these cells either. These results indicate that BET through the activation of Nrf2 and subsequent induction of the expression of genes controlled by this factor may exert its hepatoprotective and anticarcinogenic effects. Moreover, the activation of mitogen-activated protein kinases may be responsible for the activation of Nrf2 in the THLE-2 cells.

scholarly journals The Therapeutic Effect of Curcumin in Quinolinic Acid-Induced Neurotoxicity in Rats is Associated with BDNF, ERK1/2, Nrf2, and Antioxidant Enzymes

Antioxidants ◽  
2019 ◽  
Vol 8 (9) ◽  
pp. 388 ◽  
Author(s):  
Ricardo A. Santana-Martínez ◽  
Carlos A. Silva-Islas ◽  
Yessica Y. Fernández-Orihuela ◽  
Diana Barrera-Oviedo ◽  
José Pedraza-Chaverri ◽  
...  
Keyword(s):  
Therapeutic Effect ◽  
Quinolinic Acid ◽  
Antioxidant Defense System ◽  
Mitogen Activated Protein Kinase ◽  
Motor Deficit ◽  
Related Factor ◽  
Morphological Alterations ◽  
Protein Levels ◽  
Mitogen Activated Protein ◽  
Neurotropic Factor

In the present study we investigated the participation of brain-derived neurotropic factor (BDNF) on the activation of the mitogen activated protein kinase (MAPK) protein extracellular signal-regulated kinase-1/2 (ERK1/2) as a mechanism of curcumin (CUR) to provide an antioxidant defense system mediated by the nuclear factor erythroid 2-related factor 2 (Nrf2) in the neurotoxic model induced by quinolinic acid (QUIN). Wistar rats received CUR (400 mg/kg, intragastrically) for 6 days after intrastriatal injection with QUIN (240 nmol). CUR improved the motor deficit and morphological alterations induced by QUIN and restored BDNF, ERK1/2, and Nrf2 levels. CUR treatment avoided the decrease in the protein levels of glutathione peroxidase (GPx), glutathione reductase (GR), γ-glutamylcysteine ligase (γ-GCL), and glutathione (GSH) levels. Only, the QUIN-induced decrease in the GR activity was prevented by CUR treatment. Finally, QUIN increased superoxide dismutase 2 (SOD2) and catalase (CAT) levels, and the γGCL and CAT activities; however, this increase was major in the QUIN+CUR group for γ-GCL, CAT, and SOD activities. These data suggest that the therapeutic effect of CUR could involve BDNF action on the activation of ERK1/2 to induce increased levels of protein and enzyme activity of antioxidant proteins regulated by Nrf2 and GSH levels.

scholarly journals Angelicae Gigantis Radix Regulates LPS-Induced Neuroinflammation in BV2 Microglia by Inhibiting NF-κB and MAPK Activity and Inducing Nrf-2 Activity

Molecules ◽  
2019 ◽  
Vol 24 (20) ◽  
pp. 3755 ◽  
Author(s):  
You-Chang Oh ◽  
Yun Hee Jeong ◽  
Wei Li ◽  
Younghoon Go
Keyword(s):  
Nitric Oxide ◽  
High Performance ◽  
Mitogen Activated Protein Kinase ◽  
Inflammatory Factors ◽  
Related Factor ◽  
Nuclear Factor ◽  
Mapk Activity ◽  
Mitogen Activated Protein ◽  
Bv2 Microglia ◽  
Oxide Synthase

Angelicae Gigantis Radix (AGR) has been widely used as a traditional medicine in East Asia. The effects of AGR on neuroinflammation have not previously been studied in detail. In the study presented here, we investigated the antineuroinflammatory properties of this herb and its mechanism of operation. The effects of AGR on neuroinflammation were studied by measuring the production of inflammatory factors and related enzymes, and analyzing the expression levels of proteins and genes involved its activity, in lipopolysaccharide (LPS)-stimulated BV2 microglia. We found that AGR pretreatment strongly inhibits the production of nitric oxide (NO), cytokines, and the enzymes inducible nitric oxide synthase (iNOS), and cyclooxygenase (COX)-2, and effectively induces the activation of heme oxygenase (HO)-1 and its regulator, nuclear factor erythroid 2-related factor 2 (Nrf-2). We also found that AGR effectively regulates the activation of nuclear factor (NF)-κB and mitogen-activated protein kinase (MAPK). We confirmed the antineuroinflammatory effects of the main constituents of the plant as identified by high-performance liquid chromatography (HPLC). Our results indicate that the neuroinflammation inhibitory activity of AGR occurs through inhibition of NF-κB and MAPK and activation of Nrf-2.

scholarly journals The Neuroprotective Role of Polydatin: Neuropharmacological Mechanisms, Molecular Targets, Therapeutic Potentials, and Clinical Perspective

Molecules ◽  
2021 ◽  
Vol 26 (19) ◽  
pp. 5985
Author(s):  
Sajad Fakhri ◽  
Mohammad Mehdi Gravandi ◽  
Sadaf Abdian ◽  
Esra Küpeli Akkol ◽  
Mohammad Hosein Farzaei ◽  
...  
Keyword(s):  
Side Effects ◽  
Protein Kinase ◽  
Spinal Cord Injuries ◽  
Plant Secondary Metabolites ◽  
Antioxidant Response ◽  
Nuclear Factor Κb ◽  
Mitogen Activated Protein Kinase ◽  
Related Factor ◽  
Mitogen Activated Protein ◽  
Antioxidant Response Elements

Neurodegenerative diseases (NDDs) are one of the leading causes of death and disability in humans. From a mechanistic perspective, the complexity of pathophysiological mechanisms contributes to NDDs. Therefore, there is an urgency to provide novel multi-target agents towards the simultaneous modulation of dysregulated pathways against NDDs. Besides, their lack of effectiveness and associated side effects have contributed to the lack of conventional therapies as suitable therapeutic agents. Prevailing reports have introduced plant secondary metabolites as promising multi-target agents in combating NDDs. Polydatin is a natural phenolic compound, employing potential mechanisms in fighting NDDs. It is considered an auspicious phytochemical in modulating neuroinflammatory/apoptotic/autophagy/oxidative stress signaling mediators such as nuclear factor-κB (NF-κB), NF-E2–related factor 2 (Nrf2)/antioxidant response elements (ARE), matrix metalloproteinase (MMPs), interleukins (ILs), phosphoinositide 3-kinases (PI3K)/protein kinase B (Akt), and the extracellular regulated kinase (ERK)/mitogen-activated protein kinase (MAPK). Accordingly, polydatin potentially counteracts Alzheimer’s disease, cognition/memory dysfunction, Parkinson’s disease, brain/spinal cord injuries, ischemic stroke, and miscellaneous neuronal dysfunctionalities. The present study provides all of the neuroprotective mechanisms of polydatin in various NDDs. Additionally, the novel delivery systems of polydatin are provided regarding increasing its safety, solubility, bioavailability, and efficacy, as well as developing a long-lasting therapeutic concentration of polydatin in the central nervous system, possessing fewer side effects.

Mifepristone-inducible recombinant adenovirus attenuates paraquat-induced lung injury in rats

2014 ◽  
Vol 34 (1) ◽  
pp. 32-43 ◽  
Author(s):  
G-L Hong ◽  
Q-Q Cai ◽  
J-P Tan ◽  
X-Z Jiang ◽  
G-J Zhao ◽  
...  
Keyword(s):  
Lung Injury ◽  
Recombinant Adenovirus ◽  
Antioxidant Response ◽  
Nuclear Factor Κb ◽  
Heme Oxygenase 1 ◽  
Related Factor ◽  
Dependent Manner ◽  
Nuclear Factor ◽  
Quinone Oxidoreductase ◽  
Protein Levels

Objective: To investigate the effects of overexpression of nuclear factor E2-related factor-2 (NRF2) on lung injury in rats exposed to paraquat (PQ) poisoning. Methods: A mifepristone (RU486)-inducible recombinant adenoviral vector carrying the human NRF2 gene (Ad-RUNRF2) was constructed and transfected via airway into the rats 7 days before the administration of RU486. Rats were orally challenged with PQ at 20 mg/kg 24 h after the injection of RU486. On days 0.5, 3 and 21 after PQ poisoning, the expressions of NRF2 and cytokines related to inflammation and oxidation in lung tissue were examined. Results: RU486 remarkably enhanced NRF2 mRNA and NRF2 protein levels in Ad-RUNRF2-transfected rats in a dose-dependent manner ( p < 0.01). PQ stimulated compensatory overexpression of NRF2, heme oxygenase 1 (HO-1) and NAD(P)H quinone oxidoreductase 1 (NQO-1) in lungs on days 0.5 and 3 after exposure ( p < 0.05), but depleted the expression of catalase (CAT), glutathione peroxidase (GSH-Px) and glutathione (GSH), with an increased malondialdehyde (MDA) ( p < 0.05). However, pretreatment with Ad-RUNRF2 and RU486 strongly enhanced the expression levels of NRF2, HO-1, NQO-1, CAT and GSH-Px in the lungs of PQ intoxicated rats, with increased GSH and decreased MDA ( p < 0.05). Pretreatment with Ad-RUNRF2 and RU486 also strongly suppressed the PQ-induced activation of nuclear factor κB (NF-κB) and decreased the levels of tumour necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and interleukin-6 (IL-6). In addition, Ad-RUNRF2 and RU486 induction significantly reduced PQ-induced pathological changes in lungs and attenuated lung oedema and protein leakage caused by PQ ( p < 0.05). Conclusion: RU486-induced overexpression of NRF2 in lungs transfected with Ad-RUNRF2 can ameliorate PQ-induced lung injury by the activation of the NRF2-antioxidant response element (ARE) pathway.

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