In vitro Production of Interleukin-1, Interleukin-6 and Tumor Necrosis Factor-Alpha by Different Blood Cells in Patients on Intermittent Peritoneal Dialysis

Nephron ◽  
1998 ◽  
Vol 79 (2) ◽  
pp. 217-218
Author(s):  
Nada Dimkovic
Keyword(s):  
Peritoneal Dialysis ◽  
Blood Cells ◽  
Tumor Necrosis ◽  
Interleukin 1 ◽  
In Vitro Production ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Vitro Production ◽  
Necrosis Factor

scholarly journals Interleukin-1 and tumor necrosis factor alpha inhibit repair of the porcine meniscus in vitro

2007 ◽  
Vol 15 (9) ◽  
pp. 1053-1060 ◽  
Author(s):  
A. Hennerbichler ◽  
F.T. Moutos ◽  
D. Hennerbichler ◽  
J.B. Weinberg ◽  
F. Guilak
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Interleukin 1 ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Necrosis Factor

scholarly journals Activation of PPARγ Inhibits TLR4 Signal Transduction Pathway in Melanoma Cancer In Vitro

2020 ◽  
Vol 10 (3) ◽  
pp. 458-463
Author(s):  
Nasim Dana ◽  
Golnaz Vaseghi ◽  
Shaghayegh Haghjooy Javanmard
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Interleukin 1 ◽  
Necrosis Factor Alpha ◽  
Melanoma Cancer ◽  
Anticancer Effects ◽  
Factor Alpha ◽  
Tlr4 Signaling Pathway ◽  
Necrosis Factor

Purpose : Although peroxisome proliferator-activated receptor γ (PPARγ) is known as a regulator of fatty acid storage, fat cell differentiation, glucose and lipid metabolism, recent studies show that PPARγ has anticancer effects. The mechanisms of PPARγ activation in melanoma cancer remain unclarified. Recently, increased TLR4 expression has been associated with the melanoma cancer progression. We investigated whether the anti-cancer effect of PPARγ is through regulating TLR4 signaling pathway. Methods: Mouse melanoma cells (B16F10) were treated in different groups: control, pioglitazone (1, 10, 100, 300 µmol/L), lipopolysaccharide (LPS) (5 µg/mL) and LPS + pioglitazone. In another experiment, they were treated with CLI-095 (1 μM), and after 1 hour pioglitazone was added and subsequently stimulated with LPS. MTT assay was performed to measure the cell viability in vitro. The expression of Tlr4, Myd88, Nf-κb genes were evaluated by quantitative reverse transcription PCR (qRT-PCR) in different groups. The concentration of tumor necrosis factor alpha and Interleukin 1 beta in the cell culture medium were measured by enzyme-linked immunosorbent assay (ELISA) kits. Results: We show that activation of PPARγ by its agonist, pioglitazone, reduces cell proliferation, Tlr-4, Myd-88, Nf-kb mRNA expression, and tumor necrosis factor-alpha (TNF-α) production but not interleukin-1 β (IL-1β) in B16F10 LPS–stimulated cells in vitro. Moreover, treatment of B16F10 cells with TLR4 inhibitor prior treatment with pioglitazone indicate that the anticancer effects of pioglitazone on melanoma cells was dependent on TLR4. Conclusion: The results indicate that pioglitazone has a beneficial protective effect against melanoma by affecting the TLR4 signaling pathway.

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