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Fig. 4 | BMC Complementary and Alternative Medicine

Fig. 4

From: The neuritogenic and neuroprotective potential of senegenin against Aβ-induced neurotoxicity in PC 12 cells

Fig. 4

a The variance between the expression of Gap-43 positive neurites in NGF positive controlled growth and Aβ-induced toxicity. After 7 days of growth cells were treated with or without 10 μm Aβ (25–35) for 4 days and then fixed and marked with Gap-43 and examined by immunofluorescence. In the absence of Aβ, neurites retain optimal growth and higher cell differentiation. *P < 0.001 vs. amyloid-β treatment group. b The variance between the expression of MAP2 positive neurites in NGF positive controlled growth and Aβ-induced toxicity following the same protocol as above (see a). In the absence of Aβ neurites retain optimal growth and higher cell differentiation. *P < 0.001 vs. amyloid-β treatment group. c The variance between the expression of MAP2 positive neurites in NGF and senegenin treated groups after Aβ-induced atrophy. After 7 days of growth cells were treated with or without 10 μm Aβ (25–35) for 4 days. Subsequently, NGF and senegenin were introduced for an additional 4 days to incite regeneration. Next, the cells were fixed and marked with MAP2 and examined by immunofluorescence. In the presence of senegenin neurites expressed a higher protein level and a more significant outgrowth. **P < 0.01 vs. amyloid-β & NGF treatment groups. *P < 0.05 vs. amyloid-β treatment group. *aP < 0.01 vs. amyloid-β treatment group. d The effects of senegenin on neuritogenesis after Aβ(25–35)-induced atrophy. PC 12 cells were differentiated for 7 days in the presence of NGF and were then treated with or without Aβ. 4 days after incubation with Aβ cells were treated with senegenin at concentrations of 1 μg & 5 μg/ml or NGF (100 ng/ml). Following an additional 4 days of treatment, the cells were then fixed and immunostained for phosphorylated Gap-43 as a neurite marker. The quantity, average length and maximum lengths were measured and compared. *aP < 0.05 vs. NGF treatment group. *bP < 0.05 vs. amyloid-β, NGF and 5 μg treatment groups. *cP < 0.01 vs. amyloid-β, NGF and 1 μg treatment groups. e The differences in the efficacy of drug treatments aimed at neuritogenesis were measured following the protocol mentioned above, with 1 μg/ml evincing a marked effect. *P < 0.05 vs. NGF treatment. * *P < 0.05 vs. 5 μg senegenin and NGF treatments

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