Table 3.

Comparison of the therapeutic effect between aFGF and bFGF in SCI

	aFGF	bFGF
Neuron	Stimulated neurotransmitter (Rab‐GDI) and restrained inhibitor (RKIP) of the Raf/MEK/ERK pathway to create favourable conditions for the regeneration process of neurons 73, 74	Inhibited ER stress and excessive autophagy by activating PI3K/Akt/GSK‐3β, ERK1/2 pathway and PI3K/Akt/mTOR pathway for reducing neurons apoptosis 29, 30, 90
Gliocyte	Inhibited of the production of CSPG and KSPG, component of glia scar, which secreted by astrocyte and macrophage, respectively 55, 57, 58, 64	Disrupted the production of myelin to induce reactive change of oligodendrocyte progenitor cells and increase in accumulation of microglia 100
Anti‐inflammation	Treatment of aFGF markedly induced the production of NGF, BDNF 68 and also enhanced BDNF‐expressing M2 macrophages, which promoted axonal growth and overcome inhibitory substrates within grafted nerves 69	Stimulated astrogliosis and induced astrocyte migration by activating JNK and ERK or FAK signalling pathways to minimize the spread of damage and inflammation 56, 58, 92, 93, 94, 95
Proliferation, differentiation and regeneration	Combined with schwann cell guidance channels/peripheral nerve grafts to decrease the dieback of corticospinal tract and promote the regeneration and sprouting of axon 55, 61, 70	Induced the differentiation of bone marrow mesenchymal stem cells (MSCs) 80 and dedifferentiation of mature oligodendrocyte to an immature stare 32, 76, 79. Increased the number of proliferating progenitor cells and enhanced the proliferation of ependymal cells 82, 83