Table 3.
Studies related to the effect of flavonoids on the animal model.
| Disease | Clinical Onsets | Behavioral Onsets | Disease Model | Flavonoids | Dose | Effect of Flavonoids Treatment on the Animal Model | Ref. |
|---|---|---|---|---|---|---|---|
| Alzheimer’s disease (AD) | Presence of extracellular neuritic plaques containing (Aβ) peptide and intracellular neurofibrillary tangles containing tau | AD results in a progressive loss of cognitive ability and eventually daily function activities | 5 × FAD model | 7,8-dihydroxyflavone (7,8-DHF) | IP injection (5 mg/kg) | Improved memory | [160] |
| Oral administration (5 mg/kg/day) | Improvement in memory and reduction in synapse loss | [161] | |||||
| 2 × FAD model | Apigenin | Oral administration (40 mg/kg/day) | Improvement in learning and memory, reduction in deposition of insoluble Aβ | [162] | |||
| 1 × FAD model, 3 × FAD model, SAMP8 mice | Nobiletin | IP injection (10 mg/kg) | Improvement in memory and reduction in levels of both soluble and insoluble Aβ | [163] | |||
| IP injections (10 and 30 mg/kg) | Improvement in memory; reduction in soluble Aβ levels | [164] | |||||
| 1 × FAD model | Baicalein | IP injections 10 and 50 mg/kg | Improves the memory, reduces some markers of oxidative stress | [162] | |||
| (SAMP8) | Quercetin | IP injections (10 mg/kg) | Improves working memory and reduces the production of Aβ | [165] | |||
| Oral administration (25 mg/kg/day) | Reduces the markers of oxidative stress, LPO and activates the ERK pathway | ||||||
| Huntington’s disease (HD) | Presence of a trinucleotide repeat (CAG) that encodes an abnormally long polyglutamine tract in the huntingtin protein | Movement and psychiatric disturbances, as well as cognitive impairment | 3-NP model of HD in rats | Chrysin | Oral administration (50 mg/kg/day) | Improvement in behavior and reduction in markers of oxidative stress and cell death, and enhancement in the survival of striatal neurons | [166] |
| R6/1 N-terminal transgenic mouse model | 7,8-DHF | Oral administration (5 mg/kg/day) | Delay the development of motor and cognitive deficits, prevention of the loss of striatal volume, enhances the marker of neurotrophic factor signaling, and reduction in some markers of inflammation | [167] | |||
| 3-NP model | Quercetin | oral administration (25 mg/kg/day) | Reduce motor deficits, improve mitochondrial function, and attenuate some markers of oxidative stress | [168] | |||
| R6/1 N-terminal transgenic mouse model | Anthocyanins | 100 mg/kg/day | Delay the loss of motor function | [169] | |||
| 3-NP model in rats | Hesperidin | Oral administration (100 mg/kg/day) | Reduce motor deficits, as well as markers of inflammation and oxidative stress | [170] | |||
| Amyotrophic Lateral Sclerosis (ALS) | Heritable gene mutations | Loss of the motor neurons that control the voluntary movement of muscles, resulting in paralysis and death | SOD1-G93A model | 7,8-DHF | IP injection (5 mg/kg) | Reduction in the age-dependent decrease in motor performance and preserving the total motor neuron count and dendritic spine density on motor neurons | [171] |
| Fisetin | Oral administration (9 mg/kg) | Delay the development of motor deficits, reduction in their rate of progression, and increases lifespan | [172] | ||||
| (−)-epigallocatechin gallate (EGCG) | oral administration (5.8–10 mg/kg) | Delay symptom onset and extend the lifespan | [173] |