Figures de recherche

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 Diagram

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.

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

Fig. 2 Effects of ciprofloxacin and levofloxacin in microglia cell viability. Microglia were cultured for 24 h in 10% serum-containing medium, which was replaced with serum-free medium before pre-treatment with (a, c, e) ciprofloxacin (CPFX) and (b, d, f)

Figure 5 Chart

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.

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

Fig. 3 Effects of ciprofloxacin and levofloxacin on cytokine release from LPS-stimulated cortical microglia. Microglia were subcultured for 24 h in 10% FBS-containing medium, which was replaced with serum-free medium before pretreatment with (a, c) ciprof

Figure 6 Chart

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

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

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 ciprofloxa

Figure 7 Chart

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

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

Fig. 5 Effects of ciprofloxacin and levofloxacin on LPS binding and LPS-induced TLR4 dimerization. Ba/F3 cells expressing TLR4-Flag (TLR4-F), TLR4-GFP (TLR4-G), MD2-Flag, and CD14 were pretreated with 500 μg/ml ciprofloxacin (CPFX) or levofloxacin (LVFX)

Figure 8 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.

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

Fig. 6 Model depicting cascade of the anti-inflammatory effect of ciprofloxacin and levofloxacin, targeting TLR4–MD-2 complex. LBP facilitates transfer of LPS monomers to CD14, which subsequently shifts the endotoxin to TLR4/MD-2 complex, then leading to

Figure 9 Diagram

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

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

$Figure 1. Western blot analyses of protein markers in fractions 1–6 from NSL, PD and PDi brain cortices. Equal amounts of total protein were used for NSL, PD and iPD samples. Standard molecular weight values are indicated (left).$

Figure 1 Photograph

Western blot analyses of protein markers across density gradient fractions from control, Parkinson's disease, and incidental PD brain cortices reveal altered lipid raft protein distribution.

Severe alterations in lipid composition of frontal cortex lipid rafts from Parkinson's …

Figure 2 Chart

Lipid composition analyses comparing raft and non-raft fractions between control and Parkinson's disease frontal cortex samples show significant alterations in cholesterol and sphingolipid content.

Severe alterations in lipid composition of frontal cortex lipid rafts from Parkinson's …

Figure 4. (A) Comparative analyses of main lipid classes and fatty acid contents and relevant indices between control and PD frontal cortex gray matter. Results are expressed as percent of change versus NSL group. Eight cases were analyzed in each group.

Figure 3 Chart

Comparative analyses of main lipid classes and fatty acid content between control and PD frontal cortex gray matter reveal disease-associated shifts in polyunsaturated fatty acid profiles and raft lipid indices.

Severe alterations in lipid composition of frontal cortex lipid rafts from Parkinson's …

Figure 1. The biosynthesis of melatonin.

Figure 5 Diagram

Biosynthetic pathway of melatonin from tryptophan is displayed, showing the sequential enzymatic steps through serotonin N-acetyltransferase and hydroxyindole-O-methyltransferase.

Dietary Sources and Bioactivities of Melatonin.

Figure 2. Melatonin and its metabolites.

Figure 6 Diagram

Melatonin and its metabolites including 6-hydroxymelatonin, AFMK, and AMK are structurally depicted, illustrating the biotransformation cascade.

Dietary Sources and Bioactivities of Melatonin.

Figure 3. Mechanisms of melatonin enhancing the sensitivities of lung cancer cells to berberine (B).

Figure 7 Diagram

Mechanisms by which melatonin enhances lung cancer cell sensitivity to berberine are diagrammed, showing synergistic effects on apoptotic and autophagic pathways.

Dietary Sources and Bioactivities of Melatonin.

Figure 3 Photograph

Brain imaging studies demonstrate that elevated homocysteine is associated with accelerated rates of brain atrophy, particularly in medial temporal lobe structures critical for memory. B-vitamin treatment appears to slow this atrophy in individuals with elevated baseline homocysteine.

Homocysteine and Dementia: An International Consensus Statement.

Fig. 1. Hypothetical ‘sufﬁcient causes’ for dementia that involve raised plasma total homocysteine (tHcy) as one of the single component causes. For example, B might be age, C hypercholesterolemia, D hypertension, E smoking, F ApoE4, G low physicalactivit

Figure 4 Diagram

A causal model illustrates how elevated plasma homocysteine may contribute to dementia through multiple pathways, interacting with other risk factors such as age, hypercholesterolemia, and genetic predisposition. No single factor is sufficient alone; rather, combinations of component causes drive disease.

Homocysteine and Dementia: An International Consensus Statement.

Figure 5 Forest Plot

Meta-analyses of cohort studies consistently indicate that elevated homocysteine is associated with approximately doubled risk of Alzheimer's disease. The strength of this association persists after adjustment for common confounders including age, sex, and education.

Homocysteine and Dementia: An International Consensus Statement.

Figure 1. Overview of the key anti-inﬂammatory actions of EPA and DHA. DHA, docosahexaenoic acid; EPA, eicosapentaenoic acid; NFκB, nuclear factor kappa-light-chain-enhancer of activated B cells; PPAR, peroxisome proliferator activated receptor; TLR, toll

Figure 5 Diagram

Key anti-inflammatory actions of EPA and DHA include suppression of NF-kB activation, reduction of pro-inflammatory eicosanoid production, inhibition of NLRP3 inflammasome activation, and promotion of regulatory T-cell differentiation through PPAR-gamma signaling.

Expert Opinion on Benefits of Long-Chain Omega-3 Fatty Acids (DHA and EPA) …

Figure 1 Acanthocytes. Peripheral blood smear showing acanthocytosis in a patient with McLeod syndrome (May Gruenwald-Giemsa; x100; scale bar = 10 μm).

Figure 12 Micrograph

Peripheral blood smear from a patient with McLeod syndrome reveals acanthocytosis, characterized by irregularly spiculated red blood cells. May Gruenwald-Giemsa staining at 100x magnification (scale bar = 10 micrometers) highlights the distinctive thorny morphology of these erythrocytes.