**Figure 7.** Fig. 4 Effects of ciprofloxacin and levofloxacin on NF-κB activation in unstimulated and LPS-stimulated microglia. Cells were subcultured for 24 h in 10% serum-containing medium, which was replaced with serum-free medium before stimulation with ciprofloxacin (CPFX) and levofloxacin (LVFX) (500 μg/ml) ± 100 ng/ml LPS. a Cells were processed for NF-κB p65 immunostaining. Experiments were performed three times and representative confocal images showing subcellular localization of p65 are shown. Scale bars, 10 μm. b Fluorescence intensity profiles along an ideal oriented line across a representative cell (yellow arrows in the third line of (a)). c The fluorescence intensity of cytoplasmic and nuclear p65 subunit was calculated using ImageJ software and results are presented as a percentage of nuclear (gray bars) over cytoplasmic NF-κB p65 (white bars). Data are mean ± SEM from five random fields of three separate experiments

Açıklama

NF-kB nuclear translocation in LPS-stimulated microglia is attenuated by both ciprofloxacin and levofloxacin, as shown by immunofluorescence or reporter gene assays.

More Figures from This Paper

Figure 4

Molecular docking analysis reveals two alternative binding conformations of ciprofloxacin within the TLR4-MD-2 complex binding pocket, suggesting direct physical interaction with the innate immune receptor.

diagram

Figure 5

Cell viability assays demonstrate that ciprofloxacin and levofloxacin at the tested concentrations do not significantly reduce microglial survival, confirming that anti-inflammatory effects are not due to cytotoxicity.

chart

Figure 6

Cytokine release profiles from LPS-stimulated cortical microglia reveal dose-dependent reductions in TNF-alpha and IL-6 following fluoroquinolone treatment.

chart

Figure 8

LPS binding and TLR4 dimerization assays in Ba/F3 cells demonstrate that fluoroquinolones interfere with the initial receptor activation step of innate immune signaling.

chart

Figure 9

Proposed mechanistic model depicts how ciprofloxacin and levofloxacin target the TLR4-MD-2 complex to block LPS-induced downstream signaling cascades and cytokine production.

diagram

Figure 7

Chart

682 × 611px · 283,3 KB

Source Paper

Ciprofloxacin and levofloxacin attenuate microglia inflammatory response via TLR4/NF-kB pathway.

Journal of neuroinflammation (2019)

PMID: 31319868

DOI: 10.1186/s12974-019-1538-9

Cite This Figure

![Figure 7: NF-kB nuclear translocation in LPS-stimulated microglia is attenuated by both ciprofloxacin and levofloxacin, as shown by immunofluorescence or reporter gene assays.](https://pdfs.citedhealth.com/figures/31319868/105.png)

> Source: Morena Zusso et al. "Ciprofloxacin and levofloxacin attenuate microglia inflammatory response via TLR." *Journal of neuroinflammation*, 2019. PMID: [31319868](https://pubmed.ncbi.nlm.nih.gov/31319868/)

<figure>
  <img src="https://pdfs.citedhealth.com/figures/31319868/105.png" alt="NF-kB nuclear translocation in LPS-stimulated microglia is attenuated by both ciprofloxacin and levofloxacin, as shown by immunofluorescence or reporter gene assays." />
  <figcaption>Figure 7. NF-kB nuclear translocation in LPS-stimulated microglia is attenuated by both ciprofloxacin and levofloxacin, as shown by immunofluorescence or reporter gene assays.<br>  Source: Morena Zusso et al. "Ciprofloxacin and levofloxacin attenuate microglia inflammatory response via TLR." <em>Journal of neuroinflammation</em>, 2019. PMID: <a href="https://pubmed.ncbi.nlm.nih.gov/31319868/">31319868</a></figcaption>
</figure>

İlgili Kanıtlar

Curcumin için Oxidative Stress & Neuroinflammation

Derece B · 15 çalışma