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Brilliant Blue FCF | Ref. |
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In vitro assays | Phosphatases activities modulation | PTP1B function | IC50 = 91 µM | [21] |
YPTP1 function | IC50 > 120 µM |
Selective pannexin-1 activity inhibition | IC50 = 0.27 µM | [43] |
Mitochondrial respiration inhibition | [22] |
|
In vivo assays | Food and Drug Administration (FDA) oral absorption limits | 12 mg/kg/day | [22] |
Higher gastrointestinal permeability in sepsis | Systemic absorption enteral feedings after tracheostomy for obstructive apnea | [22] |
Systemic absorption chronic renal failure | [22] |
It leads to death | [85] |
No evident alterations (even in carcinogenicity studies) in the animal models used | [86, 87] |
Increase in important hepatic health-indicative enzymes | Alanine transaminase, aspartate transaminase, alkaline phosphatase, and bilirubin | [88] |
|
Brilliant Blue R | |
|
In vitro assays | Biochemical analyses and protein quantitation in protein-dye binding assays | [23–26] |
Electrophoresis studies microscopy | [31–33] |
Polyacrylamide gels in electrophoresis | [30] |
|
Brilliant Blue G | |
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In vitro assays | Biochemical analyses and protein quantitation | [23–26] |
The administration of BBG reduced the agglomeration of pathogenic prion protein (PrPres) in vitro | [73] |
Electrophoresis studies | [31–33] |
Microscopy studies | [34, 35] |
Polyacrylamide gels in electrophoresis | [30] |
Bradford assay | [36] |
Virus-like particles purification | [37] |
P2X7R noncompetitive antagonist | IC50 = 12 nM (rat) | [10] |
IC50 = 265 nM (human) | [10] |
P2X7-induced calcium influx | pIC50 < 4 (mouse) pIC50 = 5.09 (rat) pIC50 < 4 (human) | [96] |
P2X7-associated pore formation (Yopro-1 uptake) | pIC50 = 6.71 (BALB/c mouse) pIC50 = 6.34 (C57BL/6 mouse) pIC50 = 6.24 (rat) pIC50 = 5.71 (human) | [96] |
Pannexin-1 antagonist | Oocytes-expressing Pannexin-1-induced ionic currents | IC50 ~ 3 µM | [97] |
|
In vivo assays | Ophthalmic procedures | [54, 55] |
Visualization of anatomical structures during vitreoretinal surgery | [57] |
Vitreoretinal surgical procedures | [58] |
Deleterious consequences of ATP release following brain injury | Microglial activation in the rat nucleus accumbens (NAc) | [59] |
Inhibition of ATP-induced caspase-3 activity |
Traumatic spinal cord injury | Local astrocytes and microglia activity inhibition | [60] |
Inhibition of neutrophil infiltration |
Huntington’s disease (HD) | BBG impaired the symptomatology (body weight loss, motor-coordination deficits, and neuronal apoptosis) | [61] |
Seltzer model of neuropathic pain | Acute thermal nociception | [62] |
Freund’s adjuvant (CFA) pain model | Moderate effect in inflammatory pain and edema |
BBG toxicity assays in Drosophila melanogaster | No impairment on survival of the insect model (LC50 = 38 mM). No neurotoxic effects | [63] |
Suppression of P2X7R-induced ganglion cell death | [64] |
Protective neuronal effects upon oxygen-glucose deprivation | The brain damaged area following ischemia was diminished in the animals pretreated with BBG, compared to treatment with vehicle alone | [67] |
Cerebral ischemia/reperfusion (I/R) injury | BBG (10 μg) protected against transient global cerebral I/R injury, augmented survival rates, retarded I/R-induced learning and memory deficits, and suppressed I/R-induced neuronal death, DNA cleavage, glial activation and inflammatory cytokine overexpression in the hippocampus | [68] |
Traumatic brain injury (TBI) induced by posterior cerebral edema | BBG (25 mg/kg) orally administered before the TBI induction diminished the TBI effects | [69] |
Duchenne muscular dystrophy (mdx/mdx mouse) | BBG treatment recovered the CD62L in blood lymphocytes and it maintained its ability to migrate to the heart | [71] |
Treatment with BBG impaired the number of degeneration-regeneration cycles in mdx skeletal muscles in vivo | [72] |
Agglomeration of pathogenic prion protein (PrPres) | Diminished number of PrPres in infected mouse brain after the administration of BBG | [73] |
Chronic renal dysfunctions renal injury induced by hypertension | BBG suppressed the diuresis pressure threshold in F344 rats | [78] |
Amyotrophic lateral sclerosis (ALS) | The administration of BBG inhibited the progression of ALS | [79] |
|