Table 1.

Licochalcone A as a neuroprotective compound.

Row	Reference	Experimental Model	Main Findings
1	[56]	Molecular docking and Molecular dynamics simulations	Licochalcone A lead to a conformational disruption of the Aβ(1–42) protofibril.
2	[57]	SH-SY5Y cells	Licochalcone A shows a neuroprotective effect against Aβ-induced neurotoxicity, 5–35 inhibiting oxidative stress, mitochondrial dysfunction, and apoptosis. The proposed mechanism is through the activation of the PI3K/Akt/mTOR signaling pathway in SH-SY5Y cells.
3	[15]	Tet-On Aβ-GFP293/SH-SY5Y cells	Licochalcone A reduce oxidative stress, activate CREB-dependent BDNF/AKT/ERK signaling pathway involved in cell survival and CREB-dependent BCL2 for antiapoptosis.
4	[15,57,58,59]	Aβ-GFP 293/SH-SY5Y/RAW 264.6/BV-2 cells.	Licochalcone A ameliorate Aβ-induced aggregation, oxidative stress and promote neurite outgrowth in neuron like cells. Likewise, Licochalcone A prevents microglia-mediated inflammation.
5	[60]	Kainic Acid (model of temporal lobe epilepsy)	Inhibition of JNK1 by Licochalcone A can prevent neuronal degeneration in a mice experimental model of temporal lobe epilepsy TLE.
6	[61]	Rat primary cortical neurons culture	Neuroprotective properties of Licochalcone A against oxygen-glucose deprivation/reperfusion in cortical neurons could be explained trough the activation of the SIRT1/Nrf2 signaling and the inhibition of downstream NF-κB signaling pathway
7	[62]	Rat primary microglia culture	Licochalcone A exerts anti-neuroinflammatory and anti-oxidative effects in primary rat microglia mainly dependent on the arachidonic acid/COX-2/PGE2 pathway.
8	[63]	Lipopolysaccharide (LPS)-induced PD models in vivo and in vitro	Licochalcone A inhibits LPS-induced microglial activation via downregulation the activation of ERK1/2 and NF-κB p65 pathways. Licochalcone A treatment prevents dopaminergic neurodegeneration by inhibiting microglia-mediated neuroinflammation.
9	[64]	Neuropathic pain in a rat model.	Licochalcone A exerts protective effects against CCI-evoked neuropathic pain in rat model, through inhibiting microglia activation, p38 phosphorylation and inflammatory response.