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Neuritogenic effect of standardized extract of Centella asiatica ECa233 on human neuroblastoma cells.

Wanakhachornkrai O, Pongrakhananon V, Chunhacha P, Wanasuntronwong A, Vattanajun A, Tantisira B, Chanvorachote P, Tantisira MH - BMC Complement Altern Med (2013)

Bottom Line: While ECa 233 had only limited effects on cell viability, it significantly enhanced neurite outgrowth of IMR-32 cells at the concentrations of 1-100 μg/ml.ERK1/2 and Akt signaling pathways seemed to account for the neurotrophic effect observed.In conjunction with in vivo neuroprotective effect of ECa 233 previously reported, the results obtained support further development of ECa 233 for clinical use in neuronal injury or neurodegenerative diseases.

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ABSTRACT

Background: In order to gain insight into neuroprotective effects of ECa 233, a standardized extract of Centella asiatica, previously demonstrated in animal models of memory impairment induced by transient global ischemia or intracerebroventricular injection of β-amyloid, the effect of ECa 233 on neurite outgrowth of human IMR-32 neuroblastoma cell line was investigated.

Methods: Cells were seeded and incubated with various concentrations of ECa 233. Morphometric analysis was carried out by a measurement of the longest neurite growth of cells at 24 and 48 h. Contributing signaling pathways possibly involved were subsequently elucidated by western blot analysis.

Results: While ECa 233 had only limited effects on cell viability, it significantly enhanced neurite outgrowth of IMR-32 cells at the concentrations of 1-100 μg/ml. Western blot analysis revealed that ECa 233 significantly upregulated the level of activated ERK1/2 and Akt of the treated cells suggesting their involvement in the neuritogenic effect observed, which was subsequently verified by the finding that an addition of their respective inhibitors could reverse the effect of ECa 233 on these cells.

Conclusions: The present study clearly demonstrated neurite outgrowth promoting activity of ECa 233. ERK1/2 and Akt signaling pathways seemed to account for the neurotrophic effect observed. In conjunction with in vivo neuroprotective effect of ECa 233 previously reported, the results obtained support further development of ECa 233 for clinical use in neuronal injury or neurodegenerative diseases.

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Representative photomicrograph of IMR-32 cells using phase contrast. (A) non-treated control, (B) BDNF 100 ng/ml, (C-F) ECa 233 0.1, 1, 10 and 100 μg/ml respectively (scale bar = 50 μm). Cells treated with BDNF and ECa 233 at the concentrations of 1, 10 and 100 μg/ml showed relatively longer neurite length.
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Figure 2: Representative photomicrograph of IMR-32 cells using phase contrast. (A) non-treated control, (B) BDNF 100 ng/ml, (C-F) ECa 233 0.1, 1, 10 and 100 μg/ml respectively (scale bar = 50 μm). Cells treated with BDNF and ECa 233 at the concentrations of 1, 10 and 100 μg/ml showed relatively longer neurite length.

Mentions: The non-cytotoxic and non-proliferative concentrations of ECa 233 at 0.1, 1, 10 and 100 μg/ml were further used in neurite outgrowth experiments. BDNF, a well-known trophic factor of neurite extension and neuronal survival was used as a positive control. We found that the addition of 100 ng/ml BDNF to the cells caused dramatic increase of the neurite outgrowth (Figure 2B). Likewise, cells treated with ECa 233 at the concentrations of 1, 10 and 100 μg/ml exhibited increased length of neurite compared to those of non-treated control (Figure 2D-F).


Neuritogenic effect of standardized extract of Centella asiatica ECa233 on human neuroblastoma cells.

Wanakhachornkrai O, Pongrakhananon V, Chunhacha P, Wanasuntronwong A, Vattanajun A, Tantisira B, Chanvorachote P, Tantisira MH - BMC Complement Altern Med (2013)

Representative photomicrograph of IMR-32 cells using phase contrast. (A) non-treated control, (B) BDNF 100 ng/ml, (C-F) ECa 233 0.1, 1, 10 and 100 μg/ml respectively (scale bar = 50 μm). Cells treated with BDNF and ECa 233 at the concentrations of 1, 10 and 100 μg/ml showed relatively longer neurite length.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3750251&req=5

Figure 2: Representative photomicrograph of IMR-32 cells using phase contrast. (A) non-treated control, (B) BDNF 100 ng/ml, (C-F) ECa 233 0.1, 1, 10 and 100 μg/ml respectively (scale bar = 50 μm). Cells treated with BDNF and ECa 233 at the concentrations of 1, 10 and 100 μg/ml showed relatively longer neurite length.
Mentions: The non-cytotoxic and non-proliferative concentrations of ECa 233 at 0.1, 1, 10 and 100 μg/ml were further used in neurite outgrowth experiments. BDNF, a well-known trophic factor of neurite extension and neuronal survival was used as a positive control. We found that the addition of 100 ng/ml BDNF to the cells caused dramatic increase of the neurite outgrowth (Figure 2B). Likewise, cells treated with ECa 233 at the concentrations of 1, 10 and 100 μg/ml exhibited increased length of neurite compared to those of non-treated control (Figure 2D-F).

Bottom Line: While ECa 233 had only limited effects on cell viability, it significantly enhanced neurite outgrowth of IMR-32 cells at the concentrations of 1-100 μg/ml.ERK1/2 and Akt signaling pathways seemed to account for the neurotrophic effect observed.In conjunction with in vivo neuroprotective effect of ECa 233 previously reported, the results obtained support further development of ECa 233 for clinical use in neuronal injury or neurodegenerative diseases.

View Article: PubMed Central - HTML - PubMed

ABSTRACT

Background: In order to gain insight into neuroprotective effects of ECa 233, a standardized extract of Centella asiatica, previously demonstrated in animal models of memory impairment induced by transient global ischemia or intracerebroventricular injection of β-amyloid, the effect of ECa 233 on neurite outgrowth of human IMR-32 neuroblastoma cell line was investigated.

Methods: Cells were seeded and incubated with various concentrations of ECa 233. Morphometric analysis was carried out by a measurement of the longest neurite growth of cells at 24 and 48 h. Contributing signaling pathways possibly involved were subsequently elucidated by western blot analysis.

Results: While ECa 233 had only limited effects on cell viability, it significantly enhanced neurite outgrowth of IMR-32 cells at the concentrations of 1-100 μg/ml. Western blot analysis revealed that ECa 233 significantly upregulated the level of activated ERK1/2 and Akt of the treated cells suggesting their involvement in the neuritogenic effect observed, which was subsequently verified by the finding that an addition of their respective inhibitors could reverse the effect of ECa 233 on these cells.

Conclusions: The present study clearly demonstrated neurite outgrowth promoting activity of ECa 233. ERK1/2 and Akt signaling pathways seemed to account for the neurotrophic effect observed. In conjunction with in vivo neuroprotective effect of ECa 233 previously reported, the results obtained support further development of ECa 233 for clinical use in neuronal injury or neurodegenerative diseases.

Show MeSH
Related in: MedlinePlus