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] |