Table 2.

Therapeutic effects and potential pathways of jujube in the prevention and treatment for neurological diseases.

Diseases	Models	Type	Administration	Effects	Refs.
Cerebral ischemia	Rats and gerbils: I/R, MACo	In vivo	i.g.: 100 mg/kg 100, 250, 500 mg/kg	↑SOD ↑BDNF, NeuN-immunoreactive neurons ↓Reactive gliosis ↓HNE, MDA, NO ↓Neurological deficit score, motor dysfunction, cerebral infarct volume	[29,30]
AD	Rats and mice: scopolamine, D-galactose, NBM	In vivo	p.o.: 16, 32 mg/d (oleamide) 1 14–16 mg/d 29, 57, 114 mg/kg	↑Learning and memory ↑SOD, FRAP, GSH ↑ACh ↑Neurons ↓ALT, AST, AChE, BChE, GFAP, Iba-1 ↓Caspase3, 9 ↓IL-1β, TNF-α, IL-6, INF-β	[15,31,33]
Epilepsy	Rats: maximal electroshock, pentylenetetrazole	In vivo	i.p.: 100, 250, 500 mg/kg p.o.: 500 mg/kg	↑Learning memory ↑GSH, AChE, BChE ↓MDA ↓THLE, GTCS	[34,35]

¹ Unless stated in the table, such as oleamide extracted from jujube, the administered sample was the whole jujube fruit or its extract. The up arrow indicates that the indicator is This indicator is upgraded/increased/enhanced. On the contrary, the down arrow indicates that the indicator is downgraded/decreased/weakened. Notes: I/R, ischemia/reperfusion; MACo, middle cerebral artery occlusion; i.g., intragastric gavage; SOD, Superoxide dismutase; HNE, 4-Hydroxynonenal; MDA, malondialdehyde; NO, nitric oxide; BDNF, brain-derived neurotrophic factor; NBM, nucleus basalis of Meynert; p.o., per os; FRAP, ferric reducing/antioxidant power; GSH, glutathione; ACh, Acetylcholine; ALT, alanine aminotransferase; AST, aspartate aminotransferase; AChE, acetylcholinesterase; BChE, butyrylcholinesterase; GFAP, glial fibrillary acidic protein; Iba-1, ionized calcium-binding adapter molecule 1; IL-6, interleukin-1β; TNF-α, tumor necrosis factor-α; INF-β, interferon-β; i.p., intraperitoneal injections; THLE, tonic hindlimb extension; GTCS, generalized tonic–clonic seizures.