scholarly journals Influence of Prebiotic Activity of Agave salmiana Fructans on Mucus Production and Morphology Changes in Colonic Epithelium Cell of Healthy Wistar Rats

2021 ◽  
Vol 12 ◽  
Author(s):  
Amneris Iraida Castillo Andrade ◽  
Erika García Chávez ◽  
Cecilia Rivera Bautista ◽  
Cuauhtemoc Oros Ovalle ◽  
Miguel Angel Ruiz Cabrera ◽  
...  
Keyword(s):  
Wistar Rats ◽  
Normal Structure ◽  
Proximal Colon ◽  
Colonic Epithelium ◽  
Mucus Production ◽  
Tnf Α ◽  
Agave Salmiana ◽  
Factor Α ◽  
Cell Changes ◽  
Colonic Cells

The beneficial health of evaluating prebiotic effect by the consumption of Agave salmiana fructans (A. salmiana fructans) was assessed in the epithelium of the cecum and proximal colon of Wistar rats fed at different doses for 35 days with regards to mucus production, morphological cell changes, and the serum concentration of tumor necrosis factor-α (TNF-α). Results showed a significant increase in mucus-secreting cells (P < 0.05) and a normal structure with preserved crypts, without morphological damage to colonic cells for a dose of 12.5% (w/w) with respect to the control and the other doses evaluated. The concentration of pro-inflammatory cytokine TNF-α was decreased significantly (P < 0.05) in the groups with doses of 10 and 12.5% (w/w) at 7 and 35 days, respectively. This effect was positively correlated with the reduction of inflammation in epithelial cells. This study provides direct evidence of the effects of the A. salmiana fructans on the colonic epithelium, demonstrating that a diet supplemented with 12.5% of fructans for 35 days exerts health benefits through the strengthening of the mucosa layer, which favors the adherence of the bacterial population and suppresses inflammation.

scholarly journals THE EFFECTS OF KEFIR ON THE INFLAMATORY STATUS AND THYROID FUNCTION (EXPERIMENTAL STUDY ON WISTAR RATS AFTER EXPOSED TO CHLORPYRIFOS)

2016 ◽  
Vol 9 (5) ◽  
pp. 165 ◽  
Author(s):  
Rasipin Rasipin ◽  
Edi Dharmana ◽  
Suharyo Hadisaputro ◽  
Suhartono .
Keyword(s):  
Thyroid Function ◽  
Wistar Rats ◽  
Thyroid Dysfunction ◽  
Corn Oil ◽  
Thyroid Stimulating Hormone ◽  
Male Rats ◽  
Tnf Α ◽  
Male Wistar Rats ◽  
Α Level ◽  
Factor Α

ABSTRACTObjective: Goiter is an enlarged thyroid gland remained a health problem in the agricultural areas. Chlorpyrifos (CPF) is a pesticide widely used byfarmers. Previous studies proved that CPF exposure caused thyroid dysfunction. The objective of this study was to evaluate the effects of kefir on theinflammatory status and thyroid function in male Wistar rats after exposed to CPF using biochemical and histopathological assays.Methods: Male rats were divided into 4 groups, i.e., CPF 5+kefir (5 mg/kg+3.6 ml/200 g, respectively), CPF 5 (5 mg/kg), corn oil (CO 1 ml/200 g), andnegative control (NC: Without CPF, CO, and kefir).Results: Kefir supplementation dose 3.6 ml/200 g once a day for 28 days in the rats after exposed to CPF dose 5 mg/kg once a day for 14 days, inCPF 5+kefir as compared to CPF 5: Significantly (p<0.05) decreased serum tumor necrosis factor-α (TNF-α) level; significantly (p<0.01) maintainedserum levels of tumor growth factor-β (TGF-β) and thyroid stimulating hormone (TSH) not to decrease; not significant (p>0.05) decreased the level ofinterleukin-1β, cluster of differentiation-26 expression and level of T serum; not significant (p>0.05) maintained the level of anti-thyroid peroxidasenot to decrease; and not significant (p>0.05) increased the apoptosis index. This study suggests that CPF exposure causes the inflammatory processwhich leads to thyroid dysfunction.4Conclusion: Kefir supplementation significantly decreased the level of TNF-α and maintained the levels of TGF-β and TSH not to decrease, possible toreduce the inflammatory and thyroid dysfunction processes caused by exposure to CPF in experimental animals.Keywords: Kefir, Chlorpyrifos, Inflammation, Thyroid function. 

scholarly journals Tumor Necrosis Factor-α Triggers Mucus Production in Airway Epithelium through an IκB Kinase β-dependent Mechanism

2005 ◽  
Vol 280 (43) ◽  
pp. 36510-36517 ◽  
Author(s):  
José M. Lora ◽  
Dong Mei Zhang ◽  
Sha Mei Liao ◽  
Timothy Burwell ◽  
Anne Marie King ◽  
...  
Keyword(s):  
Airway Epithelium ◽  
Transforming Growth Factor ◽  
Mucus Production ◽  
Transforming Growth Factor Α ◽  
Iκb Kinase ◽  
Tnf Α ◽  
Factor Α

Excessive mucus production by airway epithelium is a major characteristic of a number of respiratory diseases, including asthma, chronic bronchitis, and cystic fibrosis. However, the signal transduction pathways leading to mucus production are poorly understood. Here we examined the potential role of IκB kinase β (IKKβ) in mucus synthesis in vitro and in vivo. Tumor necrosis factor-α (TNF-α) or transforming growth factor-α stimulation of human epithelial cells resulted in mucus secretion as measured by MUC5AC mRNA and protein. TNF-α stimulation induced IKKβ-dependent p65 nuclear translocation, mucus synthesis, and production of cytokines from epithelial cells. TNF-α, but not transforming growth factor-α, induced mucus production dependent on IKKβ-mediated NF-κB activation. In vivo, TNF-α induced NF-κB as determined by whole mouse body bioluminescence. This activation was localized to the epithelium as revealed by LacZ staining in NF-κB-LacZ transgenic mice. TNF-α-induced mucus production in vivo could also be inhibited by administration into the epithelium of an IKKβ dominant negative adenovirus. Taken together, our results demonstrated the important role of IKKβ in TNF-α-mediated mucus production in airway epithelium in vitro and in vivo.

scholarly journals Effectiveness of Mesenchymal Stem Cells and Bovine Colostrum on Decreasing Tumor Necrosis Factor-Α Levels and Enhancement of Macrophages M2 in Remnant Liver

2021 ◽  
Vol 9 (A) ◽  
pp. 1195-1202
Author(s):  
Ezra Endria Gunadi ◽  
Yan Wisnu Prajoko ◽  
Agung Putra
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Tumor Necrosis ◽  
Wistar Rats ◽  
Tumor Necrosis Factor Α ◽  
Bovine Colostrum ◽  
Control Group ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

BACKGROUND: Mesenchymal stem cells (MSCs) and bovine colostrum are potential therapies for the treatment of various degenerative and immune diseases. AIM: This study aimed to analyze the effect of MSCs on levels of tumor necrosis factor-Α (TNF-α) and macrophages M2 in the liver fibrosis of Wistar rats after 50% resection. METHODS: This study is a quasi-experimental post-test-only control group design to analyze the effect of giving bovine colostrum and MSCs to test animals on the process of regeneration of the remaining 50% liver with fibrosis. The study was conducted at the Stem Cell and Cancer Research Universitas Sultan Agung. The number of samples used was 40 male Wistar rats. The independent variables included MSC 1.000.0000 cells and bovine colostrum at a dose of 15 μL/g. Dependent variables used were macrophages M2 and levels of TNF-α ELISA. RESULTS: TNF-α levels on day 3 were (p = 0.001), day 7 were (p = 0.01), and day 10 were (p = 0.01) in liver tissue in various study groups analyzed using ELISA on day three*. The results showed differences which were significant between the control and treatment groups (p < 0.05). The expression of CD163 marked brown in liver tissue had more expression than the control group. CONCLUSION: The combination of MSCs and bovine colostrum can reduce TNF-α levels and significantly increase macrophages expression in the liver fibrosis of Wistar rats after 50% resection on the 3th, 7th, and 10th days.

Evaluation of the protective effect of paricalcitol and vitamin D3 at doxorubicin nephrotoxicity in rats with 99mTechnetium-dimercaptosuccinic acid renal scintigraphy and biochemical methods

2020 ◽  
pp. 096032712095001
Author(s):  
Fadime Demir ◽  
Mustafa Demir ◽  
Hatice Aygun
Keyword(s):  
Tumor Necrosis ◽  
Wistar Rats ◽  
Tumor Necrosis Factor Α ◽  
Biochemical Parameter ◽  
Dimercaptosuccinic Acid ◽  
Control Groups ◽  
Tnf Α ◽  
Factor Α ◽  
Nephroprotective Effect ◽  
Necrosis Factor

Aim: The present study aimed to examine the effect of paricalcitol (PRC) and vitamin D3 (vit D3) on doxorubicin (DOX)-induced nephrotoxicity in rats. Materials and Methods: Forty-two Wistar rats were randomly categorized into six groups: control; 2) PRC(0.5 µg/kg) and 3) vit D3(5.000 IU/kg) administered for 14 days; 4) DOX, 18 mg/kg administered on the 12th, 13th and 14th days of the study; 5) PRC (0.5 µg/kg, +DOX(18 mg/kg); vit D3(5.000 IU)+DOX(18 mg/kg). On the 15th day of the experiment, 99mTc-DMSA uptake level and biochemical parameter in serum and tissue were assay. Results: Activities of 99mTechnetium-Dimercaptosuccinic Acid (99mTc-DMSA) were lower in groups receiving DOX and/or PRC+DOX, vit D3+DOX than in control groups. The 99mTc-DMSA level in the group PRC+DOX and vit D3+DOX were importantly higher than DOX group. DOX caused an important increase in blood urea nitrogen (BUN), creatinine, Tumor Necrosis Factor-α(TNF- α), interleukin-6(IL-6) and nitric oxide(NO) levels compared to control groups. However, PRC and vit D3 pretreatments lowered them. Uptake of 99mTc-DMSA level was higher in groups PRC+DOX than in vit D3+DOX group. Administration of PRC and vit D3 alone did not change alterations all of parameters. Conclusion: The results indicated that PRC administration protects kidney in DOX-induced nephrotoxic rats. In addition, PRC has a stronger nephroprotective effect than vit D3.

Genetic Variation in TNF-α, its Relation with Inflammatory Biomarkers and Susceptibility to Rheumatoid Arthritis

2020 ◽  
Vol 2 (2) ◽  
Author(s):  
Khadiga Ahmed Ismail
Keyword(s):  
Rheumatoid Arthritis ◽  
Serum Level ◽  
Functional Disability ◽  
Serum Levels ◽  
Amplification Refractory Mutation System ◽  
Reactive Protein ◽  
Tnf Α ◽  
Mutation System ◽  
Potential Factor ◽  
Factor Α

Background: Tumor necrosis Factor-α (TNF-α) is encoded and controlled by TNF-α gene, which is involved in rheumatoid arthritis (RA) susceptibility. This research aimed to identify genetic variations of TNF-α (G308A) and to establish its association with inflammatory markers in Rheumatoid Arthritis predisposition. Methods: In the present study, fifty RA patients and fifty volunteers were involved and evaluated for the C-reactive protein, rheumatoid factor, and TNF-α were estimated by ELISA, Erythrocyte Sedimentation Rate (ESR) by Wintergreen method and for TNF-α-308 G>A polymorphism by polymerase chain reaction with amplification refractory mutation system (PCR-ARMS). Results: The CRP, RF, ESR and TNF-α were significantly elevated in RA patients relative to controls. The serum level TNF-α was also significantly elevated in female patients and in patients ≥50 years. Analysis of TNF-308 gene polymorphism revealed that GG genotypes were more prevalent in RA patients than in the healthy individuals and that GG genotype may be a potential factor to RA. The G allele was more common in RA than in the control. Elevated TNF-α serum levels were significantly associated the GG genotype and functional disability in RA patients. Conclusion: TNF-α promoter 308polymorphism GG genotype may be considered as a risk factor for RA and the TNF-α serum level was significantly related to the functional disability in the disease.

Synthesis of Novel 8-Hydroxyquinoline Derivatives through Mannich Reaction and their Biological Evaluation as Potential Immunomodulatory Agents

2020 ◽  
Vol 16 (4) ◽  
pp. 531-543
Author(s):  
Shaheen Faizi ◽  
Tahira Sarfaraz ◽  
Saima Sumbul ◽  
Almas Jabeen ◽  
Sobia A. Halim ◽  
...  
Keyword(s):  
Mannich Reaction ◽  
Aromatic Aldehydes ◽  
Mannich Bases ◽  
Biological Evaluation ◽  
Mechanism Of Inhibition ◽  
Potent Inhibition ◽  
Tnf Α ◽  
Elisa Technique ◽  
Factor Α ◽  
New Compounds

Background: In continuation of our work on Mannich reaction on 8-hydroxyquinoline, fifteen different combinations of aromatic aldehydes and aniline were subjected to Mannich reaction from which twelve products (eight Mannich bases, two imines and two intramolecularly cyclized products with benzofuranone skeleton) were obtained. Among them six compounds (1, 2, 6, 8, 9 and 12) are the new compounds. The structures of the compounds were characterized by UV, IR, MS and 1H NMR. Method: The compounds were tested for the inhibition of pro-inflammatory cytokines tumor necrosis factor-α (TNF-α) and Interleukin-1β (IL-1β) at a concentration of 25 µg/mL. The cytokines were produced by THP-1 cells differentiated with PMA for 24hrs and stimulated with LPS for 4 hrs and supernatant were analyzed through ELISA technique. Results and Discussion: Compounds 1-5, 8 and 9 inhibited the production of TNF-α and IL-1β. Compounds 1, 3, and 8 exerted potent inhibitions of TNF-α with 71%, 71%, and 83% inhibition, respectively. Compounds 1 and 8 significantly inhibited the production of IL-1β with 64% and 78% inhibition, respectively. Conclusion: Compounds 1 and 8 significantly inhibited the production of IL-1β with 64% and 78% inhibition, respectively. Notably compound 8 showed the most potent inhibition of these cytokines. Additionally, the effect of compounds on viability of THP-1 cells was also evaluated. Moreover, molecular docking was carried out to study the mechanism of inhibition of TNF-α production.

Molecular Mechanisms of Curcumin in Neuroinflammatory Disorders: A Mini Review of Current Evidences

2019 ◽  
Vol 19 (3) ◽  
pp. 247-258 ◽  
Author(s):  
Mahsa Hatami ◽  
Mina Abdolahi ◽  
Neda Soveyd ◽  
Mahmoud Djalali ◽  
Mansoureh Togha ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
English Language ◽  
Molecular Mechanisms ◽  
Randomized Clinical Trials ◽  
Mitochondrial Dynamics ◽  
Nuclear Factor Κb ◽  
General Term ◽  
Neuroinflammatory Disease ◽  
Tnf Α ◽  
Factor Α

Objective: Neuroinflammatory disease is a general term used to denote the progressive loss of neuronal function or structure. Many neuroinflammatory diseases, including Alzheimer’s, Parkinson’s, and multiple sclerosis (MS), occur due to neuroinflammation. Neuroinflammation increases nuclear factor-κB (NF-κB) levels, cyclooxygenase-2 enzymes and inducible nitric oxide synthase, resulting in the release of inflammatory cytokines, such as interleukin-6 (IL-6), interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α). It could also lead to cellular deterioration and symptoms of neuroinflammatory diseases. Recent studies have suggested that curcumin (the active ingredient in turmeric) could alleviate the process of neuroinflammatory disease. Thus, the present mini-review was conducted to summarize studies regarding cellular and molecular targets of curcumin relevant to neuroinflammatory disorders. Methods: A literature search strategy was conducted for all English-language literature. Studies that assessed the various properties of curcuminoids in respect of neuroinflammatory disorders were included in this review. Results: The studies have suggested that curcuminoids have significant anti- neuroinflammatory, antioxidant and neuroprotective properties that could attenuate the development and symptom of neuroinflammatory disorders. Curcumin can alleviate neurodegeneration and neuroinflammation through multiple mechanisms, by reducing inflammatory mediators (such as TNF-α, IL-1β, nitric oxide and NF-κB gene expression), and affect mitochondrial dynamics and even epigenetic changes. Conclusion: It is a promising subject of study in the prevention and management of the neuroinflammatory disease. However, controlled, randomized clinical trials are needed to fully evaluate its clinical potential.

scholarly journals Anti-Inflammatory Effect of Simonsinol on Lipopolysaccharide Stimulated RAW264.7 Cells through Inactivation of NF-κB Signaling Pathway

Molecules ◽  
2020 ◽  
Vol 25 (16) ◽  
pp. 3573
Author(s):  
Lian-Chun Li ◽  
Zheng-Hong Pan ◽  
De-Sheng Ning ◽  
Yu-Xia Fu
Keyword(s):  
Nitric Oxide ◽  
Signaling Pathway ◽  
Morphological Changes ◽  
Raw264.7 Cells ◽  
Enzyme Linked Immunosorbent Assay ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Factor Α ◽  
Oxide Synthase ◽  
Necrosis Factor

Simonsinol is a natural sesqui-neolignan firstly isolated from the bark of Illicium simonsii. In this study, the anti-inflammatory activity of simonsinol was investigated with a lipopolysaccharide (LPS)-stimulated murine macrophages RAW264.7 cells model. The results demonstrated that simonsinol could antagonize the effect of LPS on morphological changes of RAW264.7 cells, and decrease the production of nitric oxide (NO), tumor necrosis factor α (TNF-α), and interleukin 6 (IL-6) in LPS-stimulated RAW264.7 cells, as determined by Griess assay and enzyme-linked immunosorbent assay (ELISA). Furthermore, simonsinol could downregulate transcription of inducible nitric oxide synthase (iNOS), TNF-α, and IL-6 as measured by reverse transcription polymerase chain reaction (RT-PCR), and inhibit phosphorylation of the alpha inhibitor of NF-κB (IκBα) as assayed by Western blot. In conclusion, these data demonstrate that simonsinol could inhibit inflammation response in LPS-stimulated RAW264.7 cells through the inactivation of the nuclear transcription factor kappa-B (NF-κB) signaling pathway.

#50 Gestational exposure of tumor necrosis factor-α (TNF-α) inhibitor drugs

2019 ◽  
Vol 88 ◽  
pp. 149-150 ◽  
Author(s):  
Erkoseoglu Ilknur ◽  
Kadioglu Mine ◽  
Cavusoglu Irem ◽  
Sisman Mulkiye ◽  
Aran Turhan ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Gestational Exposure ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

A direct requirement of nuclear factor-κB for suppression of apoptosis in ventricular myocytes

2000 ◽  
Vol 279 (3) ◽  
pp. H939-H945 ◽  
Author(s):  
Shareef Mustapha ◽  
Alla Kirshner ◽  
Danielle De Moissac ◽  
Lorrie A. Kirshenbaum
Keyword(s):  
Dna Binding ◽  
Gene Transcription ◽  
Ventricular Myocytes ◽  
Vital Staining ◽  
Fold Increase ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Cytoplasmic Factor ◽  
Tnf Α ◽  
Factor Α

Nuclear factor-κB (NF-κB) is a ubiquitously expressed cellular factor regulated by the cytoplasmic factor inhibitor protein κBα (IκBα). Activation of NF-κB by cytokines, including tumor necrosis factor-α (TNF-α), requires the phosphorylation and degradation of IκBα. An anti-apoptotic role for NF-κB has recently been suggested. In the present study, we ascertained whether death-promoting signals and apoptosis mediated by TNF-α are suppressed by NF-κB in postnatal ventricular myocytes. Stimulation of myocytes with TNF-α resulted in a 12.1-fold increase ( P < 0.01) in NF-κB-dependent gene transcription and DNA binding compared with controls. This was accompanied by a corresponding increase in the NF-κB target protein A20 as determined by Western blot analysis. Vital staining revealed that TNF-α was not cytotoxic to myocytes and did not provoke apoptosis. Adenovirus-mediated delivery of a nonphosphorylatable form of IκBα to inactivate NF-κB prevented TNF-α-stimulated NF-κB-dependent gene transcription and nuclear NF-κB DNA binding. Importantly, myocytes stimulated with TNF-α and defective for NF-κB activation resulted in a 2.2-fold increase ( P < 0.001) in apoptosis. To our knowledge, the data provide the first indication that a functional NF-κB signaling pathway is crucial for suppressing death-promoting signals mediated by TNF-α in ventricular myocytes.

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