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BrainCited

Curcumin Figures

87 figures from peer-reviewed research

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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 Prodegeneration factors including ageing, obesity and unhealthy diets could be balanced by physical activity, caloric restriction, and anti-oxidants to mitigate the onset, severity and duration of neurodegenerative diseases. AD: Alzheimer’s disea
Figure 3 Diagram

Pro-degeneration factors including aging, obesity, and unhealthy diets can be counterbalanced by physical activity, caloric restriction, and antioxidants. This diagram illustrates how these opposing influences modulate the onset, severity, and duration of neurodegenerative diseases including Alzheimer's, Parkinson's, and ALS.

Dietary habits, lifestyle factors and neurodegenerative diseases.

Figure 1
Figure 1 Diagram

Alzheimer's disease involves a complex pathological cascade initially triggered by amyloid-beta accumulation or aberrant APP processing. This figure argues for pleiotropic interventions that simultaneously target multiple pathological mechanisms rather than single molecular targets.

Why pleiotropic interventions are needed for Alzheimer's disease.

Figure 3
Figure 3 Diagram

Molecular pathways of iron metabolism and ferroptosis in the context of neurodegenerative disease. Excessive iron accumulation in neurons can trigger lipid peroxidation and cell death through ferroptotic mechanisms.

Homeostasis and metabolism of iron and other metal ions in neurodegenerative diseases.

Figure 4
Figure 4 Diagram

Schematic of copper homeostasis and cuproptosis mechanisms relevant to neurodegeneration. Copper imbalance has been implicated in the pathogenesis of Wilson's disease and may contribute to Alzheimer's disease progression.

Homeostasis and metabolism of iron and other metal ions in neurodegenerative diseases.

Figure 5
Figure 5 Diagram

Illustration of zinc and manganese transport and regulatory mechanisms in the central nervous system, highlighting how disruptions in metal ion balance may accelerate neurodegenerative processes.

Homeostasis and metabolism of iron and other metal ions in neurodegenerative diseases.

Figure 6
Figure 6 Diagram

Summary of therapeutic strategies targeting metal ion dysregulation in neurodegenerative diseases, including iron chelation, antioxidant supplementation, and metal transporter modulation.

Homeostasis and metabolism of iron and other metal ions in neurodegenerative diseases.

Figure 7
Figure 7 Diagram

Integrative model linking metal ion imbalance to multiple neurodegenerative disease mechanisms including oxidative stress, ferroptosis, cuproptosis, cellular senescence, and neuroinflammation.

Homeostasis and metabolism of iron and other metal ions in neurodegenerative diseases.

Figure 1. Gut dysbiosis promotes intestinal and systemic inflammation with consequently Aβ aggregation and neuroinflammation finally leading to neurodegeneration and Alzheimer’s disease. Abbreviations: Aβ = amyloid beta; PP = polyphenols; SCFA = short chain
Figure 6 Diagram

A pathway diagram illustrates how gut dysbiosis promotes intestinal and systemic inflammation, leading to amyloid-beta aggregation, neuroinflammation, and ultimately neurodegeneration in Alzheimer's disease. The cascade connects microbial imbalance to blood-brain barrier compromise and central nervous system pathology.

The Immunopathogenesis of Alzheimer's Disease Is Related to the Composition of Gut …

Figure 2. Change of the microbiome (e.g., by Western diet) resulting in intestinal dysbiosis leads to low grade inflammation in the gut and to increased intestinal and BBB permeability and consecutively to neuroinflammation and cognitive decline; oral patho
Figure 7 Diagram

Western diet-induced microbiome changes are mapped to intestinal dysbiosis, low-grade gut inflammation, and increased permeability of both the intestinal barrier and blood-brain barrier. The resulting systemic inflammatory state is linked to neuroinflammatory processes implicated in Alzheimer's disease progression.

The Immunopathogenesis of Alzheimer's Disease Is Related to the Composition of Gut …

Figure 1
Figure 1 Diagram

Major pharmacotherapeutic targets in Alzheimer's disease are mapped, including amyloid-beta aggregation, tau hyperphosphorylation, neuroinflammation, and cholinergic dysfunction as key intervention points.

Review of Pharmacotherapeutic Targets in Alzheimer's Disease and Its Management Using Traditional …

Figure 2
Figure 2 Diagram

The amyloid cascade hypothesis and its therapeutic targets are illustrated, showing how beta-secretase and gamma-secretase inhibitors, along with anti-amyloid antibodies, aim to reduce pathological plaque formation.

Review of Pharmacotherapeutic Targets in Alzheimer's Disease and Its Management Using Traditional …

Figure 3
Figure 3 Diagram

Tau protein pathology and potential therapeutic interventions are depicted, including kinase inhibitors and immunotherapy approaches targeting neurofibrillary tangle formation in Alzheimer's disease.

Review of Pharmacotherapeutic Targets in Alzheimer's Disease and Its Management Using Traditional …

Figure 4
Figure 4 Diagram

Neuroinflammatory pathways in Alzheimer's disease and anti-inflammatory therapeutic targets are outlined, showing microglial activation, cytokine cascades, and potential points of pharmacological intervention.

Review of Pharmacotherapeutic Targets in Alzheimer's Disease and Its Management Using Traditional …

Figure 5
Figure 5 Diagram

Traditional medicinal plants investigated for Alzheimer's management are catalogued with their bioactive compounds and proposed neuroprotective mechanisms, including antioxidant and anti-inflammatory activities.

Review of Pharmacotherapeutic Targets in Alzheimer's Disease and Its Management Using Traditional …

Figure 6
Figure 6 Diagram

Cholinergic system dysfunction in Alzheimer's disease and current cholinesterase inhibitor therapies are illustrated, showing how acetylcholine deficiency contributes to cognitive decline.

Review of Pharmacotherapeutic Targets in Alzheimer's Disease and Its Management Using Traditional …

Fig. 1. Major inflammatory pathways associated with neurological disorders and potential of curcumin in restoring these deregulated pathways have been shown.
Figure 4 Diagram

Major inflammatory pathways associated with neurological disorders and curcumin's potential to restore deregulated signaling are depicted. NF-kB, Nrf2, and inflammasome pathways are central to curcumin's neuroprotective mechanism.

Curcumin, inflammation, and neurological disorders: How are they linked?

Fig. 2. Illustrates the curcumin activity against various NDs.
Figure 5 Diagram

Curcumin activity against various neurodegenerative diseases is illustrated, spanning Alzheimer's disease, Parkinson's disease, Huntington's disease, and amyotrophic lateral sclerosis. Distinct molecular targets are engaged in each condition.

Curcumin, inflammation, and neurological disorders: How are they linked?

Fig. 3. Neuropathological features associated with commonly occurring NDs and their outcomes.
Figure 6 Diagram

Neuropathological features associated with commonly occurring neurodegenerative diseases and their clinical outcomes are depicted. Protein aggregation, neuroinflammation, and oxidative stress represent shared pathological hallmarks.

Curcumin, inflammation, and neurological disorders: How are they linked?

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