Skip to main content
BrainCited
Fig. 1 Molecular docking analysis of the two alternative binding modes between ciprofloxacin and TLR4–MD-2 complex. All atoms are voluntarily not showed. TLR4 (colored in orange) and MD-2 (colored in magenta) are represented showing their secondary struct
Figure 4. Fig. 1 Molecular docking analysis of the two alternative binding modes between ciprofloxacin and TLR4–MD-2 complex. All atoms are voluntarily not showed. TLR4 (colored in orange) and MD-2 (colored in magenta) are represented showing their secondary structure. Mg2+ ion is represented by CPK (Corey, Pauling and Koltun model) and is colored in bronze

Beschreibung

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.

More Figures from This Paper

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.

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

Figure 6

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

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

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.

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

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

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 4

Diagram
430 × 310px · 137,7 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 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.](https://pdfs.citedhealth.com/figures/31319868/83.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/31319868/83.png" alt="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." />
  <figcaption>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.<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>

Verwandte Evidenz

B
Curcumin für Oxidative Stress & Neuroinflammation

Bewertung B · 15 Studien