Nogo A Antibody - #DF8581

Figure 5 EA promotes the repair of myelin in the ischemic penumbra and inhibits the expression of Nogo-A and NgR 7 days after MCAO/R.EA treatment was performed at the LI11 and ST36 acupoints in MCAO/R rats. ANA-12 was delivered via intraperitoneal injection at 0.5 mg/kg once per day for 7 consecutive days. (A) Representative images of Luxol fast blue staining at 7 days. There was a loss of myelin in destructive lesions post-MCAO/R, demyelination was significantly reduced after EA intervention, and the outcome in the MCAO/R + ANA-12 group was worse than that in the MCAO/R group. The arrow indicates the myelin in the ischemic penumbra. Scale bars: 1000 μm (upper) and 50 μm (lower). (B) Representative immunofluorescence images of Nogo-A (green, Alexa Fluor 488) in the ischemic penumbra. Nogo-A was significantly increased in the MCAO/R group compared with the sham group, and it could be reversed by EA treatment. Green: Nogo-A; blue: DAPI. Scale bars: 20 μm and 5 μm in the enlarged part. (C) The results of the immunofluorescence examination of NgR (green, Alexa Fluor 488) in the ischemic penumbra. Blue: DAPI. NgR expression was increased in the MCAO/R group, and significantly decreased after the EA intervention. Scale bars: 20 μm and 5 μm in the enlarged part. (D–F) EA inhibited the MCAO/R-induced protein expression of Nogo-A and NgR in the ischemic penumbra cortex, as determined by western blot. (G, H) Nogo-A and NgR mRNA expression levels were detected via quantitative real-time polymerase chain reaction. Data are presented as the mean ± SD (n = 6). ##P < 0.01, vs. sham group; *P < 0.05, **P < 0.01, vs. MCAO/R group; &&P < 0.01, vs. MCAO/R + EA group (one-way analysis of variance followed by least significant difference post hoc test). The experiments were repeated 3 times. ANA-12: TrkB inhibitor; DAPI: 4,6-diamidino-2-phenylindole; EA: electroacupuncture; MCAO/R: middle cerebral artery occlusion and reperfusion; NgR: Nogo receptor; TrkB: tyrosine kinase B.

Figure 5 EA promotes the repair of myelin in the ischemic penumbra and inhibits the expression of Nogo-A and NgR 7 days after MCAO/R.EA treatment was performed at the LI11 and ST36 acupoints in MCAO/R rats. ANA-12 was delivered via intraperitoneal injection at 0.5 mg/kg once per day for 7 consecutive days. (A) Representative images of Luxol fast blue staining at 7 days. There was a loss of myelin in destructive lesions post-MCAO/R, demyelination was significantly reduced after EA intervention, and the outcome in the MCAO/R + ANA-12 group was worse than that in the MCAO/R group. The arrow indicates the myelin in the ischemic penumbra. Scale bars: 1000 μm (upper) and 50 μm (lower). (B) Representative immunofluorescence images of Nogo-A (green, Alexa Fluor 488) in the ischemic penumbra. Nogo-A was significantly increased in the MCAO/R group compared with the sham group, and it could be reversed by EA treatment. Green: Nogo-A; blue: DAPI. Scale bars: 20 μm and 5 μm in the enlarged part. (C) The results of the immunofluorescence examination of NgR (green, Alexa Fluor 488) in the ischemic penumbra. Blue: DAPI. NgR expression was increased in the MCAO/R group, and significantly decreased after the EA intervention. Scale bars: 20 μm and 5 μm in the enlarged part. (D–F) EA inhibited the MCAO/R-induced protein expression of Nogo-A and NgR in the ischemic penumbra cortex, as determined by western blot. (G, H) Nogo-A and NgR mRNA expression levels were detected via quantitative real-time polymerase chain reaction. Data are presented as the mean ± SD (n = 6). ##P < 0.01, vs. sham group; *P < 0.05, **P < 0.01, vs. MCAO/R group; &&P < 0.01, vs. MCAO/R + EA group (one-way analysis of variance followed by least significant difference post hoc test). The experiments were repeated 3 times. ANA-12: TrkB inhibitor; DAPI: 4,6-diamidino-2-phenylindole; EA: electroacupuncture; MCAO/R: middle cerebral artery occlusion and reperfusion; NgR: Nogo receptor; TrkB: tyrosine kinase B.

Fig. 6 MiR-212-5p promotes synaptic plasticity and attenuates axon degeneration at 7 days following MCAO/R. A Ultrastructures of the synapses in the ischemic penumbra analysed using TEM. Scale bar = 2 μm. B Schematic of the presynaptic (violet) and postsynaptic (green) structures. C The number of synapses in the ischemic penumbra of the cortex in each group. D Width of the synaptic space (nm). n = 3 per group. E Immunofluorescence staining shows MAP-2 (in green) expression in the ischemic penumbra of the cortex. Nuclei were stained with DAPI and are visualised in blue. Scale bar = 50 μm. F Representative images of western blots for Nogo-A, NgR, and GAP-43. G Quantitative analysis of the western blot results. n = 4–6 per group. H-J Immunofluorescence staining was performed to show the presence of Nogo-A, NgR and β III tubulin in the ischemic penumbra of the cortex. Nuclei were stained with DAPI and are visualised in blue. Scale bar =, 50 μm. The data are presented as the means ± SEM. *P 

Fig. 6 MiR-212-5p promotes synaptic plasticity and attenuates axon degeneration at 7 days following MCAO/R. A Ultrastructures of the synapses in the ischemic penumbra analysed using TEM. Scale bar = 2 μm. B Schematic of the presynaptic (violet) and postsynaptic (green) structures. C The number of synapses in the ischemic penumbra of the cortex in each group. D Width of the synaptic space (nm). n = 3 per group. E Immunofluorescence staining shows MAP-2 (in green) expression in the ischemic penumbra of the cortex. Nuclei were stained with DAPI and are visualised in blue. Scale bar = 50 μm. F Representative images of western blots for Nogo-A, NgR, and GAP-43. G Quantitative analysis of the western blot results. n = 4–6 per group. H-J Immunofluorescence staining was performed to show the presence of Nogo-A, NgR and β III tubulin in the ischemic penumbra of the cortex. Nuclei were stained with DAPI and are visualised in blue. Scale bar =, 50 μm. The data are presented as the means ± SEM. *P