Table 4.

Neuroprotective effects and underlying mechanisms of α-Bisabolol.

Neuroprotective
Compound	Dose/Route/ Duration	Model	Major Mechanisms	Reference
α-Bisabolol	5, 25, and 250 μmol/L for 7 days	Rotenone (500 μmol/L) induced neurotoxicity in Drosophila	↓ mortality and motor deficits, ↓ thiol level ↑ SOD, CAT and Keap1	[46]
α-Bisabolol	50 mg/kg i.p, 30 min before rotenone for 4 weeks	Rotenone (2.5 mg/kg) induced Parkinson’s disease	⇥ neuronal loss, ↓ MDA, ↑ GSH, SOD and CAT, ↓ glial activation, ↓ IL-1β, IL-6, TNF-α, iNOS and COX-2, ↑ Bcl-2, ↓ Bax, caspases-3, 9 and cytochrome-C, restored ATP and MC-I activity	[47]
α-Bisabolol	5, 10 μg/mL for 2 h in N2a cells and 25, 50 and 100 μg/mL in elegans	Aβ25–35 peptide (50 μM for 24 h) induced toxicity in N2a cells and Caenorhabditis elegans CL4176 and CL2006	⇥ cholinesterase and β-secretase, ↓ ROS and RNS ↓ Bax and caspase-3 ↓ ace-1, hsp-4 and Aβ genes	[49]
α-Bisabolol	5 mg/mL for 2 h	Aβ25–35 peptide (50 μM for 24 h) induced toxicity in PC12 cells	↓ Aβ aggregation ↑ cell survival	[50]
α-Bisabolol	5 and 10 μg/mL for 2 h	Aβ25–35 peptide (50 μM for 24 h) induced toxicity in Neuro-2a cells	↓ ROS and RNS, ↓ β-secretase and AchE activities, ↓ Bax, caspase3, and ↑ Bcl-2	[51]
α-Bisabolol β-D-fucopyranoside	10–50 μg/mL	Aβ25–35 (100 μM for 24 h, 48 h, 96 h, 9 d) induced toxicity in Neuro 2a cells	Inhibited AChE, ↓ H2O2 and OH•, ↓ Aβ aggregation ↑ cell survival	[52]
α-Bisabolol	50, 100 and 200 mg/kg/day, p.o	Permanent occlusion of the middle cerebral artery induced cerebral ischemia in mice	↓ infarct size, ↑ motor performance, ↑ crossings and rearings	[54]

Symbols indications: ↑; increase, ↓; decrease, ⇥; activity inhibition.