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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.

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.

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Effects of ECa 233 on cell viability and proliferation of IMR-32 cells at 24 and 48 h after applying. There was no significant difference among groups.
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Figure 1: Effects of ECa 233 on cell viability and proliferation of IMR-32 cells at 24 and 48 h after applying. There was no significant difference among groups.

Mentions: First, effect of ECa 233 on cell viability of IMR-32 cells was determined using Resazurin based assay. Cells were incubated in the presence or absence of ECa 233 (0.1, 1, 10 and 100 μg/ml) for 24 and 48 h and percentage of cell viability was determined. Percentage of such cell viability was compared among groups as well as with non-treated control (p < 0.05) (Figure 1). The results show that cell viability was 106 ± 1.6, 95.6 ± 6.44, 102.4 ± 4.03 and 104.6 ± 7.48% of control in response to ECa 233 at the concentrations of 0.1, 1, 10 and 100 μg/ml, respectively. In addition, cell viability at 48 h after treatment in all ECa 233-treated groups showed no significant change from that of non-treated control indicating that treatment with ECa 233 at the concentrations tested had neither cytotoxic nor proliferative effects on these neuroblastoma cells.


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)

Effects of ECa 233 on cell viability and proliferation of IMR-32 cells at 24 and 48 h after applying. There was no significant difference among groups.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 1: Effects of ECa 233 on cell viability and proliferation of IMR-32 cells at 24 and 48 h after applying. There was no significant difference among groups.
Mentions: First, effect of ECa 233 on cell viability of IMR-32 cells was determined using Resazurin based assay. Cells were incubated in the presence or absence of ECa 233 (0.1, 1, 10 and 100 μg/ml) for 24 and 48 h and percentage of cell viability was determined. Percentage of such cell viability was compared among groups as well as with non-treated control (p < 0.05) (Figure 1). The results show that cell viability was 106 ± 1.6, 95.6 ± 6.44, 102.4 ± 4.03 and 104.6 ± 7.48% of control in response to ECa 233 at the concentrations of 0.1, 1, 10 and 100 μg/ml, respectively. In addition, cell viability at 48 h after treatment in all ECa 233-treated groups showed no significant change from that of non-treated control indicating that treatment with ECa 233 at the concentrations tested had neither cytotoxic nor proliferative effects on these neuroblastoma cells.

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