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Prolonged oral administration of Gastrodia elata extract improves spatial learning and memory of scopolamine-treated rats.

Park YM, Lee BG, Park SH, Oh HG, Kang YG, Kim OJ, Kwon LS, Kim YP, Choi MH, Jeong YS, Oh J, Lee HY - Lab Anim Res (2015)

Bottom Line: Gastrodia elata (GE) is traditionally used for treatment of various disorders including neurodegenerative diseases such as Alzheimer's disease.In vitro assay demonstrated that 50 µM of pre-aggregated Aβ was lethal to about a half portion of PC12 cells and that Aβ aggregate-induced cell death was significantly decreased with GE treatment at ≤10 mg/mL in a dose-dependent manner.These findings suggest that a GE regimen may potentially ameliorate learning and memory deficits and/or cognitive impairments caused by neuronal cell death.

View Article: PubMed Central - PubMed

Affiliation: Huvet Co. Ltd., Iksan, Korea.

ABSTRACT
Gastrodia elata (GE) is traditionally used for treatment of various disorders including neurodegenerative diseases such as Alzheimer's disease. To investigate the neuroprotective effect of GE, amyloid-β peptide (Aβ)-treated PC12 cells were cultured with GE aqueous extract. In vitro assay demonstrated that 50 µM of pre-aggregated Aβ was lethal to about a half portion of PC12 cells and that Aβ aggregate-induced cell death was significantly decreased with GE treatment at ≤10 mg/mL in a dose-dependent manner. To further examine in vivo cognitive-improving effects, an artificial amnesic animal model, scopolamine-injected Sprague-Dawley rats, were orally administered the extract for 6 weeks followed by behavioral tests (the passive avoidance test and Morris water maze test). The results showed that an acute treatment with scopolamine (1 mg/kg of body weight) effectively induced memory impairment in normal rats and that the learning and memory capability of scopolamine-treated rats improved after prolonged administration of GE extract (50, 250 and 500 mg/kg of body weight for 6 weeks). These findings suggest that a GE regimen may potentially ameliorate learning and memory deficits and/or cognitive impairments caused by neuronal cell death.

No MeSH data available.


Related in: MedlinePlus

Protective effect of GE against Aβ-induced neural cell death. (A) Cytotoxicity of GE sample at 0, 0.01, 0.05, 0.5, 1, 5, 10, 20 and 30 mg/mL applied to PC12 cells was examined. Relative cell viability normalized to the control (100, 96, 93, 94, 95, 93, 91, 65, and 47% at each concentration) decreased in a dose-dependent manner. N=5; error bars, mean±SEM. (B) Cytotoxicity of PC12 cells treated with pre-aggregated Aβ at 0, 5, 10, 20, 40, 50, 70 and 100 µM was assayed. Relative cell viability (normalized to the control; 100% at the 0-µM-treated condition) was decreased in a dose-dependent manner, 88.3, 78.9, 77.8, 62.9, 56.8, 42.8, and 23.4% on average at each respective concentration. N=5; error bars, mean±SEM. (C) The neural cell protective effect of GE against Aβ-induced cytotoxicity was evaluated. PC12 cells were pretreated with GE at various concentrations (0-10 mg/mL) for 1 hr and cultured in the presence of 50 µM of Aβ for 48 hr. Cell viability under GE-treated conditions were significantly higher compared to controls (no GE-treated). N=7; error bars, mean±SEM.
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Figure 1: Protective effect of GE against Aβ-induced neural cell death. (A) Cytotoxicity of GE sample at 0, 0.01, 0.05, 0.5, 1, 5, 10, 20 and 30 mg/mL applied to PC12 cells was examined. Relative cell viability normalized to the control (100, 96, 93, 94, 95, 93, 91, 65, and 47% at each concentration) decreased in a dose-dependent manner. N=5; error bars, mean±SEM. (B) Cytotoxicity of PC12 cells treated with pre-aggregated Aβ at 0, 5, 10, 20, 40, 50, 70 and 100 µM was assayed. Relative cell viability (normalized to the control; 100% at the 0-µM-treated condition) was decreased in a dose-dependent manner, 88.3, 78.9, 77.8, 62.9, 56.8, 42.8, and 23.4% on average at each respective concentration. N=5; error bars, mean±SEM. (C) The neural cell protective effect of GE against Aβ-induced cytotoxicity was evaluated. PC12 cells were pretreated with GE at various concentrations (0-10 mg/mL) for 1 hr and cultured in the presence of 50 µM of Aβ for 48 hr. Cell viability under GE-treated conditions were significantly higher compared to controls (no GE-treated). N=7; error bars, mean±SEM.

Mentions: To test the cytotoxicity of GE, PC12 cells were treated with various concentrations of GE sample (0, 0.01, 0.05, 0.5, 1, 5, 10, 20 and 30 mg/mL) for 1 hr followed by cell viability assay. Results showed that ≥91% of the cells were viable at concentrations ≤10 mg/mL of GE (Figure 1A). However, average cell viabilities at 20 mg/mL and 30 mg/mL GE conditions were 65 and 47%, respectively. For further experiments, ≤10 mg/mL of GE were applied to PC12 cells.


Prolonged oral administration of Gastrodia elata extract improves spatial learning and memory of scopolamine-treated rats.

Park YM, Lee BG, Park SH, Oh HG, Kang YG, Kim OJ, Kwon LS, Kim YP, Choi MH, Jeong YS, Oh J, Lee HY - Lab Anim Res (2015)

Protective effect of GE against Aβ-induced neural cell death. (A) Cytotoxicity of GE sample at 0, 0.01, 0.05, 0.5, 1, 5, 10, 20 and 30 mg/mL applied to PC12 cells was examined. Relative cell viability normalized to the control (100, 96, 93, 94, 95, 93, 91, 65, and 47% at each concentration) decreased in a dose-dependent manner. N=5; error bars, mean±SEM. (B) Cytotoxicity of PC12 cells treated with pre-aggregated Aβ at 0, 5, 10, 20, 40, 50, 70 and 100 µM was assayed. Relative cell viability (normalized to the control; 100% at the 0-µM-treated condition) was decreased in a dose-dependent manner, 88.3, 78.9, 77.8, 62.9, 56.8, 42.8, and 23.4% on average at each respective concentration. N=5; error bars, mean±SEM. (C) The neural cell protective effect of GE against Aβ-induced cytotoxicity was evaluated. PC12 cells were pretreated with GE at various concentrations (0-10 mg/mL) for 1 hr and cultured in the presence of 50 µM of Aβ for 48 hr. Cell viability under GE-treated conditions were significantly higher compared to controls (no GE-treated). N=7; error bars, mean±SEM.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4490148&req=5

Figure 1: Protective effect of GE against Aβ-induced neural cell death. (A) Cytotoxicity of GE sample at 0, 0.01, 0.05, 0.5, 1, 5, 10, 20 and 30 mg/mL applied to PC12 cells was examined. Relative cell viability normalized to the control (100, 96, 93, 94, 95, 93, 91, 65, and 47% at each concentration) decreased in a dose-dependent manner. N=5; error bars, mean±SEM. (B) Cytotoxicity of PC12 cells treated with pre-aggregated Aβ at 0, 5, 10, 20, 40, 50, 70 and 100 µM was assayed. Relative cell viability (normalized to the control; 100% at the 0-µM-treated condition) was decreased in a dose-dependent manner, 88.3, 78.9, 77.8, 62.9, 56.8, 42.8, and 23.4% on average at each respective concentration. N=5; error bars, mean±SEM. (C) The neural cell protective effect of GE against Aβ-induced cytotoxicity was evaluated. PC12 cells were pretreated with GE at various concentrations (0-10 mg/mL) for 1 hr and cultured in the presence of 50 µM of Aβ for 48 hr. Cell viability under GE-treated conditions were significantly higher compared to controls (no GE-treated). N=7; error bars, mean±SEM.
Mentions: To test the cytotoxicity of GE, PC12 cells were treated with various concentrations of GE sample (0, 0.01, 0.05, 0.5, 1, 5, 10, 20 and 30 mg/mL) for 1 hr followed by cell viability assay. Results showed that ≥91% of the cells were viable at concentrations ≤10 mg/mL of GE (Figure 1A). However, average cell viabilities at 20 mg/mL and 30 mg/mL GE conditions were 65 and 47%, respectively. For further experiments, ≤10 mg/mL of GE were applied to PC12 cells.

Bottom Line: Gastrodia elata (GE) is traditionally used for treatment of various disorders including neurodegenerative diseases such as Alzheimer's disease.In vitro assay demonstrated that 50 µM of pre-aggregated Aβ was lethal to about a half portion of PC12 cells and that Aβ aggregate-induced cell death was significantly decreased with GE treatment at ≤10 mg/mL in a dose-dependent manner.These findings suggest that a GE regimen may potentially ameliorate learning and memory deficits and/or cognitive impairments caused by neuronal cell death.

View Article: PubMed Central - PubMed

Affiliation: Huvet Co. Ltd., Iksan, Korea.

ABSTRACT
Gastrodia elata (GE) is traditionally used for treatment of various disorders including neurodegenerative diseases such as Alzheimer's disease. To investigate the neuroprotective effect of GE, amyloid-β peptide (Aβ)-treated PC12 cells were cultured with GE aqueous extract. In vitro assay demonstrated that 50 µM of pre-aggregated Aβ was lethal to about a half portion of PC12 cells and that Aβ aggregate-induced cell death was significantly decreased with GE treatment at ≤10 mg/mL in a dose-dependent manner. To further examine in vivo cognitive-improving effects, an artificial amnesic animal model, scopolamine-injected Sprague-Dawley rats, were orally administered the extract for 6 weeks followed by behavioral tests (the passive avoidance test and Morris water maze test). The results showed that an acute treatment with scopolamine (1 mg/kg of body weight) effectively induced memory impairment in normal rats and that the learning and memory capability of scopolamine-treated rats improved after prolonged administration of GE extract (50, 250 and 500 mg/kg of body weight for 6 weeks). These findings suggest that a GE regimen may potentially ameliorate learning and memory deficits and/or cognitive impairments caused by neuronal cell death.

No MeSH data available.


Related in: MedlinePlus