Neuropharmacological Potential and Delivery Prospects of Thymoquinone for Neurological Disorders

Table 3

Protective effect of TQ in lead, arsenic, ethanol and toluene-induced neurotoxicity, radiation-induced brain damage, and morphine-induced dependence and tolerance.

Causative agents	Doses of TQ	Potential protective effects	References
Pb	20 mg/kg	Reverses endothelial lining of brain blood vessel degeneration, ischemic brain infarction, choroid plexus blood vessel congestion, chromatolysis and microglial reaction, and neuronophagia; prevents the degeneration of hippocampal and cerebellar neurons and axon demyelination	[133]
As	10 μM, 10 mg/kg, and 20 mg/kg	Alters enzymatic and biochemical markers of oxidative stress; reduces in arsenic-induced DNA damage	[135, 136]
Ethanol	25 μM	Increases Bcl-2 expression, suppresses caspase-9 and caspase-3 activation, and diminishes the PARP-1 cleavage	[138]
Toluene	50 mg/kg	Prevents the degenerative changes, shrunken cytoplasma, slightly dilated cisternae of endoplasmic reticulum, markedly swollen mitochondria with degenerated cristae, and nuclear membrane breakdown with chromatin disorganization in neurons of the hippocampus; also, caspase-3 immunoreactivity	[139, 140]
ACR	2.5, 5, and 10 mg/kg	Protection against oxidative stress	[143]
Radiation	30 mg/kg	In brain tissue, lowers the NO and ONOO (−) levels as well as NOS enzyme activity	[144]
Morphine	10 mg/kg	Reduces oxidative stress markers; prevents tolerance and dependence	[146]

Pb: lead; As: arsenic; ACR: acrylamide; Bcl-2: B-cell lymphoma 2; PARP-1: poly [ADP-ribose] polymerase 1; NO: nitric oxide; ONOO (−): peroxynitrite; NOS: nitric oxide synthases.