Effect of a nonprotein bioactive agent on the reduction of cyclooxygenase-2 and tumor necrosis factor–α in human intervertebral disc cells in vitro

2008 ◽  
Vol 9 (5) ◽  
pp. 411-418 ◽  
Author(s):  
Tatsuhiro Yoshida ◽  
Jin Soo Park ◽  
Kimiaki Yokosuka ◽  
Kotaro Jimbo ◽  
Kei Yamada ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Intervertebral Disc ◽  
Tumor Necrosis ◽  
Cyclooxygenase 2 ◽  
Enzyme Linked Immunosorbent Assay ◽  
Mrna Levels ◽  
Disc Cells ◽  
Cox 2 ◽  
Antiinflammatory Effects ◽  
Necrosis Factor

Object Neurotropin is a nonprotein extract from the inflamed skin of rabbits inoculated with vaccinia virus. In the present study the authors sought to clarify the focal antiinflammatory effects of Neurotropin in intervertebral disc cells, and these effects were compared with those induced by the selective cyclooxygenase (COX)–2 inhibitor 6-methoxy-2-naphthylacetic acid (nabumetone). Methods Six human intervertebral disc specimens were harvested during spinal surgery for lumbar disc herniation. Cells were stimulated with 500 pg/ml of interleukin (IL)–1β in the presence of various concentrations of Neurotropin (0, 10−5, 10−4, and 10−3 Neurotropin Units/ml) or 50 μg/ml of nabumetone for 3 hours. The mRNA was extracted for polymerase chain reaction (PCR), and real-time PCR was used to quantify the mRNA levels of COX- 2, tumor necrosis factor (TNF)–α, and phospholipase A2. Cyclooxygenase-2, TNFα, and prostaglandin E2 (PGE2) protein concentrations were each determined by enzyme-linked immunosorbent assay. Results Neurotropin was found to significantly suppress the expression of COX-2 and TNFα at mRNA levels as well as the concentration of COX-2 at protein levels in a dose-dependent manner. Nabumetone was found to significantly increase COX-2 at mRNA levels but directly suppress the concentration of PGE2 in culture medium. Conclusions Results in this study suggest that Neurotropin has an analgesic effect through the suppression of COX-2 and TNFα in a focal area, and nabumetone shows this same effect through the suppression of PGE2 production. Thus, Neurotropin could decrease pain by blocking the central pain pathway or increasing focal antiinflammatory effects.

scholarly journals Role of nuclear factor kappa beta, tumor necrosis factor α, and cyclooxygenase-2 in preterm labor

2015 ◽  
Vol 23 (4) ◽  
pp. 213-7
Author(s):  
Syamsul B. Riva'i ◽  
Eryati Darwin ◽  
Ellyza Nasrul ◽  
Jusuf S. Effendi
Keyword(s):  
Tumor Necrosis Factor ◽  
Preterm Labor ◽  
Tumor Necrosis ◽  
Cyclooxygenase 2 ◽  
Nuclear Factor ◽  
Nuclear Factor Kappa ◽  
Nuclear Factor Kappa Beta ◽  
Cox 2 ◽  
Term Labor ◽  
Necrosis Factor

Background: The pathway of tumor necrosis factor alpha (TNFα), nuclear factor kappa beta (NF-κB), and cyclooxygenase-2 (COX-2) activation in releasing prostaglandins is suggested to be crucial for initiating labor in the pathogenesis of preterm labor. The aim of the study was to know whether there were mean differences of NF-κB, TNFα, and COX-2 expressions between preterm and term labor and also to know the correlation among them in preterm labor.Methods: A case-control study was performed from May 2013 to February 2014 in Arifin Achmad Hospital, Pekanbaru. There were 30 subjects with preterm labor as cases and 30 with normal labor as controls. All subjects had singleton gestation with maximum parity was three, age limit of 35 year-old, and spontaneous labor in both groups. Placental tissue was collected from all subjects and evaluated with hematoxylin eosin staining. The expressions of TNFα, NF-κB, and COX-2 in the tissue were assessed with immunohistochemical staining by counting the percentage of smeared cells by two experts. The expressions of TNFα, NF-κB, and COX-2 between case and control were compared using t-test and the correlation was analyzed with Pearson correlation coefficient.Results: Mean (SD) of expressions of TNFα (93.05% [12.68] vs 49.11% [27.33]), NF-κB (42.46% [27.29] vs 13.66% [17.77]), and COX-2 (88.75% [10.86] vs 46% [30.36]) were significantly higher in the preterm labor compared to term labor (p = 0.001). There was significant correlation between TNFα and NF-κB expression (r = 0.385; p = 0.036) and no correlation was found between NF-κB and COX-2 (p = 0.982) in preterm labor.Conclusion: High expressions of TNFα, NF-κB, and COX-2 in preterm labor showed to contribute in the onset of preterm labor. High TNFα may suggest that infection was a leading cause of preterm labor. This is supported with an increase in NF-κB activation will increase COX-2 and subsequently prostaglandins that result in premature labor.

scholarly journals Attenuation of Inflammatory Events in Human Intervertebral Disc Cells With a Tumor Necrosis Factor Antagonist

Spine ◽  
2011 ◽  
Vol 36 (15) ◽  
pp. 1190-1196 ◽  
Author(s):  
S. Michael Sinclair ◽  
Mohammed F. Shamji ◽  
Jun Chen ◽  
Liufang Jing ◽  
William J. Richardson ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Intervertebral Disc ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Antagonist ◽  
Disc Cells ◽  
Factor Antagonist ◽  
Necrosis Factor

scholarly journals Mesenchymal stem cell-originated exosomal lncRNA HAND2-AS1 impairs rheumatoid arthritis fibroblast-like synoviocyte activation through miR-143-3p/TNFAIP3/NF-κB pathway

2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Yuhua Su ◽  
Yajing Liu ◽  
Chao Ma ◽  
Chunxiao Guan ◽  
Xiufen Ma ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Tumor Necrosis Factor ◽  
Western Blot ◽  
Tumor Necrosis ◽  
Cell Counting ◽  
Biological Behavior ◽  
Luciferase Reporter ◽  
Enzyme Linked Immunosorbent Assay ◽  
Binding Interaction ◽  
Necrosis Factor

Abstract Background Long non-coding RNA heart and neural crest derivatives expressed 2-antisense RNA 1 (HAND2-AS1) was found to be elevated in rheumatoid arthritis (RA) fibroblast-like synoviocytes (RA-FLSs). However, whether HAND2-AS1 functions as an exosomal lncRNA related to mesenchymal stem cells (MSCs) in RA progression is unknown. Methods The expression of HAND2-AS1, microRNA (miR)-143-3p, and tumor necrosis factor alpha-inducible protein 3 (TNFAIP3) was detected using quantitative real-time polymerase chain reaction and Western blot. Cell proliferation, apoptosis, migration, and invasion were detected using cell counting kit-8, flow cytometry, and wound healing and transwell assays. The levels of tumor necrosis factor-α (TNF-α) and interleukins (IL)-6 were analyzed using enzyme-linked immunosorbent assay. The level of phosphorylated-p65 was examined by Western blot. The binding interaction between miR-143-3p and HAND2-AS1 or TNFAIP3 was confirmed by the dual-luciferase reporter and RIP assays. Exosomes were isolated by ultracentrifugation and qualified by transmission electron microscopy (TEM), nanoparticle tracking analysis (NTA), and Western blot. Results HAND2-AS1 was lowly expressed in RA synovial tissues, and HAND2-AS1 re-expression suppressed the proliferation, motility, and inflammation and triggered the apoptosis in RA-FLSs via the inactivation of NF-κB pathway. Mechanistically, HAND2-AS1 directly sponged miR-143-3p and positively regulated TNFAIP3 expression, the target of miR-143-3p. Moreover, the effects of HAND2-AS1 on RA-FLSs were partially attenuated by miR-143-3p upregulation or TNFAIP3 knockdown. HAND2-AS1 could be packaged into hMSC-derived exosomes and absorbed by RA-FLSs, and human MSC-derived exosomal HAND2-AS1 also repressed above malignant biological behavior of RA-FLSs. Conclusion MSC-derived exosomes participated in the intercellular transfer of HAND2-AS1 and suppressed the activation of RA-FLSs via miR-143-3p/TNFAIP3/NF-κB pathway, which provided a novel insight into the pathogenesis and treatment of RA.

scholarly journals Role of arachidonic acid metabolism in transcriptional induction of tumor necrosis factor gene expression by phorbol ester.

1989 ◽  
Vol 9 (1) ◽  
pp. 252-258 ◽  
Author(s):  
J Horiguchi ◽  
D Spriggs ◽  
K Imamura ◽  
R Stone ◽  
R Luebbers ◽  
...  
Keyword(s):  
Gene Expression ◽  
Arachidonic Acid ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Leukotriene B4 ◽  
Mrna Levels ◽  
Arachidonic Acid Release ◽  
Acid Release ◽  
Tnf Gene ◽  
Necrosis Factor

The treatment of human HL-60 promyelocytic leukemia cells with 12-O-tetradecanoylphorbol-13-acetate (TPA) is associated with induction of tumor necrosis factor (TNF) transcript. The study reported here has examined TPA-induced signaling mechanisms responsible for the regulation of TNF gene expression in these cells. Run-on assays demonstrated that TPA increases TNF mRNA levels by transcriptional activation of this gene. The induction of TNF transcripts by TPA was inhibited by the isoquinolinesulfonamide derivative H7 but not by HA1004, suggesting that this effect of TPA is mediated by activation of protein kinase C. TPA treatment also resulted in increased arachidonic acid release. Moreover, inhibitors of phospholipase A2 blocked both the increase in arachidonic acid release and the induction of TNF transcripts. These findings suggest that TPA induces TNF gene expression through the formation of arachidonic acid metabolites. Although indomethacin had no detectable effect on this induction of TNF transcripts, ketoconazole, an inhibitor of 5-lipoxygenase, blocked TPA-induced increases in TNF mRNA levels. Moreover, TNF mRNA levels were increased by the 5-lipoxygenase metabolite leukotriene B4. In contrast, the cyclooxygenase metabolite prostaglandin E2 inhibited the induction of TNF transcripts by TPA. Taken together, these results suggest that TPA induces TNF gene expression through the arachidonic acid cascade and that the level of TNF transcripts is regulated by metabolites of the pathway, leukotriene B4 and prostaglandin E2.

Role of arachidonic acid metabolism in transcriptional induction of tumor necrosis factor gene expression by phorbol ester

1989 ◽  
Vol 9 (1) ◽  
pp. 252-258
Author(s):  
J Horiguchi ◽  
D Spriggs ◽  
K Imamura ◽  
R Stone ◽  
R Luebbers ◽  
...  
Keyword(s):  
Gene Expression ◽  
Arachidonic Acid ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Leukotriene B4 ◽  
Mrna Levels ◽  
Arachidonic Acid Release ◽  
Acid Release ◽  
Tnf Gene ◽  
Necrosis Factor

The treatment of human HL-60 promyelocytic leukemia cells with 12-O-tetradecanoylphorbol-13-acetate (TPA) is associated with induction of tumor necrosis factor (TNF) transcript. The study reported here has examined TPA-induced signaling mechanisms responsible for the regulation of TNF gene expression in these cells. Run-on assays demonstrated that TPA increases TNF mRNA levels by transcriptional activation of this gene. The induction of TNF transcripts by TPA was inhibited by the isoquinolinesulfonamide derivative H7 but not by HA1004, suggesting that this effect of TPA is mediated by activation of protein kinase C. TPA treatment also resulted in increased arachidonic acid release. Moreover, inhibitors of phospholipase A2 blocked both the increase in arachidonic acid release and the induction of TNF transcripts. These findings suggest that TPA induces TNF gene expression through the formation of arachidonic acid metabolites. Although indomethacin had no detectable effect on this induction of TNF transcripts, ketoconazole, an inhibitor of 5-lipoxygenase, blocked TPA-induced increases in TNF mRNA levels. Moreover, TNF mRNA levels were increased by the 5-lipoxygenase metabolite leukotriene B4. In contrast, the cyclooxygenase metabolite prostaglandin E2 inhibited the induction of TNF transcripts by TPA. Taken together, these results suggest that TPA induces TNF gene expression through the arachidonic acid cascade and that the level of TNF transcripts is regulated by metabolites of the pathway, leukotriene B4 and prostaglandin E2.

scholarly journals Relationship between serum tumor necrosis factor receptor-2 concentration and periodontal destruction in patients with type 2 diabetes: Cross-sectional study

2016 ◽  
Vol 144 (5-6) ◽  
pp. 266-272 ◽  
Author(s):  
Sanja Matic-Petrovic ◽  
Ana Pucar ◽  
Aleksandra Jotic ◽  
Biljana Milicic ◽  
Jelena Arambasic-Jovanovic ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Tumor Necrosis Factor ◽  
Surface Area ◽  
Tumor Necrosis ◽  
Periodontal Diseases ◽  
Tumor Necrosis Factor Receptor ◽  
Enzyme Linked Immunosorbent Assay ◽  
Periodontal Destruction ◽  
Necrosis Factor

Introduction. The role of tumor necrosis factor-? (TNF?) is well documented in pathogenesis of chronic periodontitis (CP) and type 2 diabetes (T2D). Considering short half-life of TNF?, tumor necrosis factor receptor-2 (TNFR2) is used as prosperous surrogate marker of TNF? activity. Objective. The aim was to detect TNFR2 serum concentration and correlate it with periodontal destruction in patients with diagnosed T2D and nondiabetics. Methods. The study included 85 patients divided into three groups: T2D + CP (group T2D, n = 34); nondiabetics + CP (Group PD, n = 27); and healthy controls (group HC, n = 24). T2D was diagnosed according to WHO criteria (2013) and periodontitis was diagnosed using International Workshop for a Classification of Periodontal Diseases and Conditions criteria (1999). TNFR2 level was measured by enzyme-linked immunosorbent assay (ELISA). Results. There was no difference in TNFR2 level among the groups (Kruskal-Wallis, p = 0.482). Significant correlation (Pearson?s correlation coefficient) was observed between clinical attachment loss (CAL) and TNFR2 concentration in PD group (rp = -0.460, p = 0.016). In T2D group, correlations were observed between TNFR2 concentration and CAL (rp = 0.363, p = 0.005) and periodontal inflamed surface area (PISA) (rp = 0.345, p = 0.046) and periodontal epithelial surface area (PESA) (rp = 0.578, p = 0.000). Conclusion. Higher concentration of TNFR2 was associated with higher CAL, PESA, and PISA scores in T2D group. Contrary to that, nondiabetics with higher values of CAL exhibited lower concentration of TNFR2, presenting potential protective effect on periodontal destruction. These results imply that diabetes may alter TNFR2 secretion originated from periodontium.

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