Table 1.

Effect of aged garlic extract (AGE) and garlic compounds on neuroblastoma.

Compound Used	Experimental Model	Main Findings	Reference
Allicin	SK-NFI, SK-N-AS, SK-N-Be, and Kelly cell lines	Induction of programmed cell death by the increase of poly (ADP-ribose) polymerase (PARP).	[13]
Allicin	SK-N-SH cell line	Induction of apoptosis by activating the p38 MAPK pathway and the release of cytochrome c.	[14]
Allicin	BALB/c-nu/nu mice	Tumour cell proliferation decreased; increase the number of CD4+, CD8+, and NK cells and IFN-γ levels in the serum; and decrease in mRNA and protein levels of VEGF.	[15]
Z-ajoene	SK-N-AS cell line	Increase active caspase-3 and p53.	[16]
SAC	LA-N-5 human NB cell line	Decrease cell proliferation.	[17]
SAC	SJ-NK-P and IMR5 cell lines	Induction of apoptosis and cell cycle arrest in the G1 phase.	[18]
AGE	SJ-NK-P and IMR5 cell lines	Decrease the mitochondrial membrane potential and increased glutathione oxidation.	[18]
DADS	SH-SY5Y cell line	Release of cytochrome c, and activation of caspase-9 in association with the activation of the JNK/c-Jun pathway.	[19]
DAS and DADS	SH-SY5Y cell line	Both compounds increase the intracellular Ca2+ and induce cell death through the release of cytochrome c.	[20]
DADS	SH-SY5Y cell line	Disruption of the cytoskeleton by Tau protein dephosphorylation.	[21]
DADS	SH-SY5Y cell line	Activation of PGC1α.	[22]
DATS	U87MG and SH-SY5Y cell line	Decrease of Bcl-2, and increased hydrogen sulfide production and ROS production.	[23]

AGE: Aged garlic extract; DADS: diallyl disulphide; DAS: diallyl sulphide; DATS: diallyl trisulfide; IFN-γ: Interferon-γ; JNK/c-Jun: c-Jun NH2-N-terminal kinase; NK: Natural killers; PGC1α: peroxisome proliferator-activated receptor-Gamma co-activator 1 alpha; ROS: reactive oxygen species; SAC: S-allylcysteine; VEGF: vascular endothelial growth factor.