scholarly journals The Protective Effect of Ceramide in Immature Rat Brain Hypoxia—Ischemia Involves Up-Regulation of BCL-2 and Reduction of TUNEL-Positive Cells

2001 ◽  
Vol 21 (1) ◽  
pp. 34-40 ◽  
Author(s):  
Yong Chen ◽  
Irene Ginis ◽  
John M. Hallenbeck
Keyword(s):  
Infarct Volume ◽  
Treated Group ◽  
Protective Role ◽  
Necrosis Factor Alpha ◽  
Immature Rat ◽  
Tnf Α ◽  
Hypoxia Ischemia ◽  
Old Rats ◽  
Factor Alpha ◽  
The Right

Preconditioning brain with tumor necrosis factor alpha (TNF-α) can induce tolerance to experimental hypoxia and stroke and ceramide is a downstream messenger in the TNF-α signaling pathway. A hypoxic-ischemic (HI) insult in the immature rat injures brain primarily through apoptosis. Apoptosis is regulated by Bcl-2 family proteins. The authors explored whether ceramide protects against HI in the immature rat, and whether Bcl-2 family protein expression is involved. Hypoxia-ischemia was produced in seven-day-old rats by ligating the right carotid artery, followed by 2 hours of 8% oxygen exposure. Thirty minutes after HI, C2-ceramide (150 μg/kg) was injected intraventricularly. Infarct volume was measured 5 days later. C2-ceramide reduced HI-induced brain damage by 45% to 65% compared with HI/dimethyl sulfoxide (DMSO) (vehicle control) or HI only groups. In separate experiments, brains of sham-operated control and HI only animals and animals subjected to HI plus C2-ceramide or DMSO infusion were sampled 6 hours, 24 hours, and 5 days after treatments and analyzed for Bcl-2, Bcl-xl, and Bax expression (Western blotting), and apoptosis (TUNEL assay). Augmented Bcl-2 and Bcl-xl levels in the C2-ceramide treated group were associated with a significant decrease in TUNEL-positive cells. The results support a protective role for ceramide in neonatal HI.

scholarly journals EKSPRESI Tumor Necrosis Factor alpha (TNF-α) DAN Transforming growth factors beta (TGF-β) PADA PERIODONTITIS APIKALIS KRONIS AKIBAT INDUKSI Enterococcus faecalis PADA TIKUS WISTAR

2019 ◽  
Vol 7 (2) ◽  
pp. 66
Author(s):  
Richard Fritzgerald ◽  
Cecilia Lunardhi ◽  
Ruslan Effendy ◽  
Tamara Yuanita
Keyword(s):  
Tissue Damage ◽  
Treated Group ◽  
Positive Control ◽  
Negative Control ◽  
Control Group ◽  
Transforming Growth Factors ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor

Background. Root canal treatment is a main role in decreasing infection from root canal and pulp. The main cause of periapical damage mostly are bacteries. E.faecalis is a bactery that is found as an etiology of endodontic treatment failure. Cell wall of this bacteria is containing Lipoteichoic acid (LTA). LTA can penetrate into the periradicular tissue, act as endotoxin in host and cause periradicular inflammation then lead to bone destruction. LTA stimulates immunology reaction that produce Tumor Necrosis Factor alpha (TNF-α) and Transforming growth factors beta (TGF-ß). TNF-α is a main mediator and also have an important role in inflamation response otherwise TGF-ß is working as a multifunction  regulator of cell growth and differentiation during reforming and remodelling.  Purpose. The aim of this study is to know about the expression of TNF-α and TGF-ß during the periapical tissue damage due to induction of E.faecalis. Method. This study used laboratory experimental with the post test only control group design. A total of 30 male rats were randomly divided into 3 main groups, Group A (control negative) : normal tooth. Group B (control positive) : every tooth was induced only by sterile BHI-b. Group C (treated group) : every tooth  was induced by 10 μl BHI-b E.faecalis ATCC212(106 CFU). The animals were sacrificed 21 days later and prepared for histological examination of tissue damage, then we did the immunohistochemistry  followed by calculation on the light microscope. Result. The analysis revealed that the expression of TNF-α at treated group are higher than negative control and positive control but the expression of  TGF-ß at treated group are higher than the negative control group but lower than positive control. Conclusion. From this study we know that the expression of TNF-α and TGF-ß are changing during the periapical tissue damage that induced by E.faecalis.

scholarly journals Immunomodulatory Activities of Sambucus javanica Extracts in DMBAExposedBALB/c Mouse

2019 ◽  
Vol 9 (4) ◽  
pp. 619-623
Author(s):  
Wira Eka Putra ◽  
Muhaimin Rifa'i
Keyword(s):  
Immune System ◽  
Tumor Necrosis Factor ◽  
Interferon Gamma ◽  
Broad Spectrum ◽  
Tumor Necrosis ◽  
Treated Group ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor

Purpose: Accumulating evidence shows the genus of Sambucus exerts a broad spectrum ofmedicinal potencies such as anticancer, antiviral, antibacterial, and antidiabetes. Based on theprevious studies, we hypothesized that bioactive compounds of Sambucus might alter severalbiological systems, including the immune system. Therefore, this study extensively aimed toevaluate the immunomodulatory activities of Sambucus javanica extracts in 7,12-dimethylbenz[a]anthracene (DMBA)-treated BALB/c mouse.Methods: The experimental mice were orally administrated with 2.8 mg.kg-1 BW of DMBA forten times within a month. After that, the mice were treated by S. javanica berries and leavesextracts for 2 weeks. Subsequently, the inflammation rate was evaluated by using flow cytometryanalysis, whereas the necrosis incidences were observed by hematoxylin & eosin staining.Results: Based on the results, we found the expression of tumor necrosis factor alpha (TNF-α)and interferon gamma (IFN-ɣ) were increased however after treated by S. javanica berries andleaves extracts were significantly decreased. In the same way, necrosis incidence was increasedin the DMBA-treated group however it was diminished with S. javanica extracts treatment.Conclusion: Together, these results suggested that S. javanica extracts have immunomodulatoryactivities to suppress inflammation and reduce necrosis incidence in experimental mice.<br />

scholarly journals Endogenous Interleukin-6 Plays a Crucial Protective Role in Streptococcal Toxic Shock Syndrome via Suppression of Tumor Necrosis Factor Alpha Production

2005 ◽  
Vol 73 (6) ◽  
pp. 3745-3748 ◽  
Author(s):  
Hongyan Diao ◽  
Masashi Kohanawa
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Interleukin 6 ◽  
Tumor Necrosis ◽  
Protective Role ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Deficient Mice ◽  
Necrosis Factor

ABSTRACT During a Streptococcus pyogenes infection in interleukin-6 (IL-6)-deficient mice, there is elevation of serum tumor necrosis factor alpha (TNF-α) levels, muscular necrosis, and death compared with infection of C57BL/6 mice. Anti-TNF-α monoclonal antibody treatment decreased mortality and muscular necrosis in the infected IL-6-deficient mice. These results suggest that IL-6 plays a crucial protective role via suppression of TNF-α production in S. pyogenes infection.

scholarly journals Sedative and Immunosuppressive Effects of Dexmedetomidine in Transplantation

2021 ◽  
Vol 14 (8) ◽  
pp. 825
Author(s):  
Chen-Fang Lee ◽  
Chih-Hsien Cheng ◽  
Hao-Chien Hung ◽  
Jin-Chiao Lee ◽  
Yu-Chiao Wang ◽  
...  
Keyword(s):  
Treated Group ◽  
Dependent Manner ◽  
Post Transplantation ◽  
Necrosis Factor Alpha ◽  
Donor Liver Transplantation ◽  
Tnf Α ◽  
Factor Alpha ◽  
Light Sedation ◽  
Dose Dependent ◽  
Adrenergic Receptor Agonist

Dexmedetomidine, an α2-adrenergic receptor agonist, is used as an anti-anxiety medication. It exerts a cholinergic effect, thereby reducing the release of tumor necrosis factor alpha (TNF-α). We hypothesized that the use of dexmedetomidine as a sedative agent in transplantation would also protect allografts. We examined our patients who underwent living donor liver transplantation. Subsequently, we generated a series of mouse models to investigate the effect of dexmedetomidine on sedation-based tolerance post transplantation. A total of 49 liver recipients were enrolled in this study, of which 23 (47%) were administered dexmedetomidine through 24 h infusion on postoperative day 1. A trend toward the improvement of hepatocyte injury along with better liver function was observed in the dexmedetomidine-treated group during the first postoperative week. In animal models, dexmedetomidine inhibited the proliferation of CD4+ and CD8+ T cells and TNF-α production in a dose-dependent manner. We used dexmedetomidine to treat skin-transplanted mice and observed a significantly prolonged graft survival in mice that were administered a higher dose of dexmedetomidine. Our results revealed that dexmedetomidine exerts a dual effect of sedation and immunosuppression. This light-sedation approach will not only make patients calmer in the intensive care unit but also protect allografts from injury.

scholarly journals Interferons Increase Cell Resistance to Staphylococcal Alpha-Toxin

2007 ◽  
Vol 76 (2) ◽  
pp. 571-577 ◽  
Author(s):  
Timur O. Yarovinsky ◽  
Martha M. Monick ◽  
Matthias Husmann ◽  
Gary W. Hunninghake
Keyword(s):  
Fatty Acid Synthase ◽  
Protective Role ◽  
Cell Resistance ◽  
Alpha Toxin ◽  
Necrosis Factor Alpha ◽  
Staphylococcal Infections ◽  
Proinflammatory Mediators ◽  
Tnf Α ◽  
Mitogen Activated Protein ◽  
Factor Alpha

ABSTRACT Many bacterial pathogens, including Staphylococcus aureus, use a variety of pore-forming toxins as important virulence factors. Staphylococcal alpha-toxin, a prototype β-barrel pore-forming toxin, triggers the release of proinflammatory mediators and induces primarily necrotic death in susceptible cells. However, whether host factors released in response to staphylococcal infections may increase cell resistance to alpha-toxin is not known. Here we show that prior exposure to interferons (IFNs) prevents alpha-toxin-induced membrane permeabilization, the depletion of ATP, and cell death. Moreover, pretreatment with IFN-α decreases alpha-toxin-induced secretion of interleukin 1β (IL-1β). IFN-α, IFN-β, and IFN-γ specifically protect cells from alpha-toxin, whereas tumor necrosis factor alpha (TNF-α), IL-6, and IL-4 have no effects. Furthermore, we show that IFN-α-induced protection from alpha-toxin is not dependent on caspase-1 or mitogen-activated protein kinases, but requires protein synthesis and fatty acid synthase activity. Our results demonstrate that IFNs may increase cell resistance to staphylococcal alpha-toxin via the regulation of lipid metabolism and suggest that interferons play a protective role during staphylococcal infections.

scholarly journals Bidirectional Concentration-Dependent Effects of Tumor Necrosis Factor Alpha in Shigella dysenteriae-Related Seizures

2003 ◽  
Vol 71 (4) ◽  
pp. 2288-2291 ◽  
Author(s):  
Yael Yuhas ◽  
Abraham Weizman ◽  
Shai Ashkenazi
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Suppressive Effect ◽  
Protective Role ◽  
Shigella Dysenteriae ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor

ABSTRACT We have previously demonstrated that pretreatment of mice with Shigella dysenteriae sonicate enhanced their susceptibility to pentylenetetrazole-induced seizures and that tumor necrosis factor alpha (TNF-α) was proconvulsive in this respect. The present study shows that TNF-α, at high concentrations, may also exert a suppressive effect on Shigella-mediated seizures. This implies that high levels of TNF-α may play a protective role in neurologic complications of S. dysenteriae infection.

Regulation of microRNAs in Inflammation-Associated Colorectal Cancer: A Mechanistic Approach

2020 ◽  
Vol 20 ◽  
Author(s):  
Sridhar Muthusami ◽  
Ilangovan Ramachandran ◽  
Sneha Krishnamoorthy ◽  
Yuvaraj Sambandam ◽  
Satish Ramalingam ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Molecular Mechanisms ◽  
Colorectal Carcinogenesis ◽  
Model Systems ◽  
Necrosis Factor Alpha ◽  
Multi Stage ◽  
Mechanistic Approach ◽  
Tnf Α ◽  
Factor Alpha

: The development of colorectal cancer (CRC) is a multi-stage process. The inflammation of the colon as in inflammatory bowel disease (IBD) such as ulcerative colitis (UC) or Crohn’s disease (CD) is often regarded as the initial trigger for the development of CRC. Many cytokines such as tumor necrosis factor alpha (TNF-α) and several interleukins (ILs) are known to exert proinflammatory actions, and inflammation initiates or promotes tumorigenesis of various cancers, including CRC through differential regulation of microRNAs (miRNAs/miRs). miRNAs can be oncogenic miRNAs (oncomiRs) or anti-oncomiRs/tumor suppressor miRNAs, and they play key roles during colorectal carcinogenesis. However, the functions and molecular mechanisms of regulation of miRNAs involved in inflammation-associated CRC are still anecdotal and largely unknown. Consolidating the published results and offering perspective solutions to circumvent CRC, the current review is focused on the role of miRNAs and their regulation in the development of CRC. We have also discussed the model systems adapted by researchers to delineate the role of miRNAs in inflammation-associated CRC.

scholarly journals Association of tumor necrosis factor-alpha -308 G/A and -238 G/A polymorphism with diabetic retinopathy: a systematic review and updated meta-analysis.

2020 ◽  
Author(s):  
Wenna Gao ◽  
Ruilin Zhu ◽  
liu yang
Keyword(s):  
Diabetic Retinopathy ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Meta Analysis ◽  
Entire Group ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor

Background: Mounting evidence has suggested tumor necrosis factor-alpha (TNF-α) can promote the development of diabetic retinopathy (DR), and TNF-α gene variants may influence DR risk. However, the results are quite different. Objectives: To comprehensively address this issue, we performed the meta-analysis to evaluate the association of TNF-α-308 G/A and -238 G/A polymorphism with DR. Method: Data were retrieved in a systematic manner and analyzed using STATA Statistical Software. Crude odds ratios (ORs) with 95% confidence intervals (CIs) were used to assess the strength of associations. Allelic and genotypic comparisons between cases and controls were evaluated. Results: For the TNF-α-308 G/A polymorphism, overall analysis suggested a marginal association with DR [the OR(95%CI) of (GA versus GG), (GA + AA) versus GG, and (A versus G) are 1.21(1.04, 1.41), 1.20(1.03, 1.39), and 1.14(1.01, 1.30), respectively]. And the subgroup analysis indicated an enhanced association among the European population. For the TNF-α-238 G/A polymorphism, there was mild correlation in the entire group [the OR(95%CI) of (GA versus GG) is 1.55(1.14,2.11) ], which was strengthened among the Asian population. Conclusion: The meta-analysis suggested that -308 A and -238 A allele in TNF-α gene potentially increased DR risk and showed a discrepancy in different ethnicities.

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