Fig. 6

Repair effect of rBM-NCPs on adult rat DRG neurons on exposure to OGD in vitro. a Phase-contrast image of neurons 6 days after culture. Scale bar, 100 μm. b Phase-contrast image showing neurons with disrupted neurites and shrinking neuron soma 8 h after OGD. Scale bar, 100 μm. c Histogram showing the relative cell viability of neurons. OGD damaged neurons 24 h after treatment with NCP-CM showed significantly increased viability compared with treatment with NM and showed equal viability compared with treatment with MSC-CM. And the increased viability of treated neurons could be inhibited by LY294002 (a blocking agent of PI3K/AKT pathway). n = 3; **p < 0.01, ***p < 0.001 compared with control group; ^#p < 0.05, ^##p < 0.01 compared with OGD+NM group; ^△△p < 0.01 compared with OGD+MSC-CM group; ^§§p < 0.01 compared with OGD+NCP-CM+LY294002 group. d Representative image showing positive expression of neural marker β-tubulin III (red) in soma and sprouting neurites of neurons in different groups. Scale bar, 100 μm. e Histograms showing the average length of the longest neurites, the ratio of neurites density to cell numbers, and the percentage of sprouting neurons with longest neurite more than double diameter of soma of neurons in different groups. n = 3; *p < 0.05, **p < 0.01, ***p < 0.001 compared with control group; ^##p < 0.01, ^###p < 0.001 compared with OGD+NM group. f Histograms showing the relative mRNA expression of trophic factors for axonal regeneration and angiogenesis by qRT-PCR analysis in normal neurons, OGD injured neurons, rBM-NCPs and rBM-MSCs, indicated EGF, CNTF, PDGFα, and VEGFα genes were higherly expressed in rBM-NCPs, as well as HGF, GDNF, NGF, and ANG genes were higherly expressed in rBM-MSCs. n = 3; *p < 0.05, **p < 0.01, ***p < 0.001 compared with normal neuron