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Table 4 Neurobiological effects produced by myricetin

From: Myricetin bioactive effects: moving from preclinical evidence to potential clinical applications

Model

Results

Ref.

Anxiety

 In vitro and in vivo

Dose-dependent reduction in lithium-induced head twitches and anxiolytic activity by altering 5-hydroxytryptamine transmission.

[80]

Alzheimer disease

 In vitro

Pro-oxidant agent and reduced the formation of ordered amyloid beta (Aβ)42 aggregation.

[81]

 In silico

Destabilizes the β-sheet ordered amyloid oligomers formed by the undecapeptide Aβ (25–35) model.

[82]

 In vitro

Marked modulation of metal-induced Aβ aggregation, more than metal-free Aβ aggregation. Increase cell survival rate of Aβ (with metal ions).

[83]

 In vitro

Increases α-secretase (ADAM10) enzyme activity and decreases of β-secretase (BACE-1). It also exerts neuroprotective activity against Aβ (1–42) with multifunctional role in counteracting AD progress.

[84]

 In vitro

Dose-dependent inhibition of α-synuclein fibrils formation and destabilization (EC50 = 0.21–1.8 μM).

[85]

 In vitro

Dose-dependent inhibition of Aβ fibrils formation from fresh Aβ (1–40) and Aβ (1–42). The EC50 value for formation, extension and destabilization Aβ fibrils ranges from 0.13–1.8 μM.

[86]

 In vivo

Increases the number of hippocampal CA3 pyramidal neurons and survival in a rat model (10 mg/kg). Improved learning and memory in a rat model with AD.

[87]

CNS

 In vitro

Reduces the aggregation of different abnormal proteins and eliminates various toxic proteins related to neurodegenerative diseases. Improves physiological functions of Hsp70 molecular chaperone and reduces mis-folded proteins.

[88]

 In vitro and in vivo

Increases GABA receptor activity via calcium channel/ CaMK-II dependent mechanism, which is distinctively different from that of most existing benzodiazepine binding site agonists of GABA receptor.

[89]

 In vivo

Increases mRNA for brain-derived neurotrophic factor (BDNF) in the hippocampus of male C57BL/6 mice at 10 and 20 mg/kg (7 days).

[90]

 In vivo

Increases BDNF concentrations in the hippocampus of male C57BL/6 mice at 50 mg/kg (21 days).

[91]

 In vivo

Enhances expression and activity of ERK1/2-CREB pathway and Na+, K+-ATPase while reduces oxidative stress level in hippocampus. Improves learning and memory when compared with D-galactose.

[92]

Epilepsy

 In vivo

Reduces seizure severity and mortality rates in mouse models and signaling pathways (BDNF-TrkB) and regulates GAD65/GABA with MMP-9 expression.

[93]

Huntington disease

 In vivo

Interacts with RNA, especially CAG motif, and decreases the huntingtin protein translation and sequestration. Reduces cytotoxicity in HD and other polyQ disease models.

[94]

Parkinson disease

 In vitro

Suppresses intracellular ROS production, re-establishes mitochondrial trans-membrane potential, and inhibits MKK4 and JNK activation.

[95]

 In vitro and in vivo

Inhibits activation of microglia (neuroinflammation), expression of pro-inflammatory mediators and reduces the number of dopaminergic neurons.

[96]

 In vivo

Dose-dependent delay in climbing ability loss, but increases the life span of flies expressing human α-synuclein in brain.

[97]

 In vivo

Prevents the loss of dopaminergic neurons and dopamine content in brain of Parkinson flies.

[98]

 In vivo

Dose-dependent inhibitory activity on α-synuclein aggregation.

[99]

 In vivo

Diminishes dopamine neuron degeneration, which is induced by 6-hydroxydopamine and 1-methyl-4-phenyl-pyridinium in substantia nigra-striatum.

[100]

  1. Aβ amyloid beta, CNS central nervous system, BDNF brain-derived neurotrophic factor