Table 2.

Roles of ginkgolides in IIR in neurological diseases.

Diseases	Actions	Ingredients	References
Neurodegenerative diseases	Inhibition of the NF-κB.	BB	Li et al. (2008)
Ischemic stroke	Decreases infarct size, serum levels of pro-inflammatory factors, expressions of intercellular adhesion molecule-2 and E-selection. Down-regulates TLR4 and NF-κB. Reduces microglial activation and promotes microglia/macrophage transferring from inflammatory M1 phenotype to M2 phenotype. Suppresses ERK/MAPK pathway and inhibits Akt phosphorylation.	GB	Gu et al. (2012)
	Reduces microglial activation and promotes microglia/macrophage transferring from inflammatory M1 phenotype to M2 phenotype.	GB	Gu et al. (2012)
	Suppresses ERK/MAPK pathway and inhibits Akt phosphorylation.	GB	Nabavi et al. (2015)
Neuroimmune diseases	Attenuates the inflammatory responses.	GB	Zhou J.-M. et al. (2016)
	Inhibits the expressions of TLR4 and MyD88.	GB	Chen et al. (2017)
	Regulates the TLR/MyD88/NF-κB.	Ginkgolides	Tran et al. (2018)

IIR, inflammatory immune response; NF-κB, nuclear factor-kappa B; BB, bilobalide; GB, ginkgolide B; TLR, toll-like receptor; ERK, extracellular regulated protein kinase; MAPK, mitogen-activated protein kinase; MyD88, myeloid differentiation factor 88.