The present study aims to investigate the effect of methanol extract of Korean mistletoe (KM; Viscum album var. coloratum), on amyloid $\beta$ protein ($A\beta$) (25-35), a synthetic 25-35 amyloid peptide, -induced neurotoxicity in cultured rat cerebral cortical neurons and mem...
The present study aims to investigate the effect of methanol extract of Korean mistletoe (KM; Viscum album var. coloratum), on amyloid $\beta$ protein ($A\beta$) (25-35), a synthetic 25-35 amyloid peptide, -induced neurotoxicity in cultured rat cerebral cortical neurons and memory impairment in mice. Exposure of cultured neurons to $10{\mu}M$$A\beta$ (25-35) for 24 h induced a neuronal cell death, which was measured by a 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl-tetrazolium bromide (MTT) assay and Hoechst 33342 staining. KM (10, 30 and $50{\mu}g/ml$) significantly inhibited the $A\beta$ (25-35)-induced apoptotic neuronal death. KM ($50{\mu}g/ml$) inhibited 10 μM Aβ (25-35)-induced elevation of intracellular calcium concentration ([Ca2+]i), which was measured by a fluorescent dye, Fluo-4 AM. Glutamate release into medium and generation of reactive oxygen species (ROS) induced by $10{\mu}M$$A\beta$ (25-35) were also inhibited by KM (10, 30 and $50{\mu}g/ml$). These results suggest that KM may mitigate the $A\beta$ (25-35)-induced neurotoxicity by interfering with the increase of [Ca2+]i and then inhibiting glutamate release and generation of ROS in cultured neurons. In addition, orally administered KM (25 and 50 mg/kg, 7 days) significantly prevented memory impairment induced by intracerebroventricular injection of $A\beta$ (25-35) (8 nmol). Taken together, it is suggested that anti-dementia effect of KM is due to its neuroprotective effect against $A\beta$ (25-35)-induced neurotoxicity and that KM may have therapeutic role in prevention of the progression of Alzheimer's disease.
The present study aims to investigate the effect of methanol extract of Korean mistletoe (KM; Viscum album var. coloratum), on amyloid $\beta$ protein ($A\beta$) (25-35), a synthetic 25-35 amyloid peptide, -induced neurotoxicity in cultured rat cerebral cortical neurons and memory impairment in mice. Exposure of cultured neurons to $10{\mu}M$$A\beta$ (25-35) for 24 h induced a neuronal cell death, which was measured by a 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl-tetrazolium bromide (MTT) assay and Hoechst 33342 staining. KM (10, 30 and $50{\mu}g/ml$) significantly inhibited the $A\beta$ (25-35)-induced apoptotic neuronal death. KM ($50{\mu}g/ml$) inhibited 10 μM Aβ (25-35)-induced elevation of intracellular calcium concentration ([Ca2+]i), which was measured by a fluorescent dye, Fluo-4 AM. Glutamate release into medium and generation of reactive oxygen species (ROS) induced by $10{\mu}M$$A\beta$ (25-35) were also inhibited by KM (10, 30 and $50{\mu}g/ml$). These results suggest that KM may mitigate the $A\beta$ (25-35)-induced neurotoxicity by interfering with the increase of [Ca2+]i and then inhibiting glutamate release and generation of ROS in cultured neurons. In addition, orally administered KM (25 and 50 mg/kg, 7 days) significantly prevented memory impairment induced by intracerebroventricular injection of $A\beta$ (25-35) (8 nmol). Taken together, it is suggested that anti-dementia effect of KM is due to its neuroprotective effect against $A\beta$ (25-35)-induced neurotoxicity and that KM may have therapeutic role in prevention of the progression of Alzheimer's disease.
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문제 정의
The present study demonstrated that methanol extract of KM significantly inhibited Aβ (25-35)-induced cultured neuronal cell death and markedly improved memory impairment induced by Aβ (25-35) in mice. As far as we know, this is the first report to demonstrate the neuroprotective effect of KM against Aβ- induced toxicity. Mistletoe has been reported to bind to microglia and AD plaque glycoproteins in human brains.
We demonstrated that KM exerted a significant inhibitory action on hydrogen peroxide-induced cultured neuronal damage.17Therefore, the aim of the present study was to investigate the protective effect of KM against Aβ (25-35)-induced neurotoxicity in cultured rat cortical neurons and impaired memory by the intracerebroventri- cular (i.c.v.) injection of Aβ (25-35) in mice.
제안 방법
18 Changes in [Ca2+]i were measured with Fluo-4 AM, a Ca2+-sensitive fluorescent dye, using a laser scanning confocal microscope (LSM 510, Carl Zeiss, Oberkochen, Germany) with 488-nm excitation argon laser and 515-nm longpass emission filters. The microfluorescence of 2’, 7’-dichlorofluorescein, the fluorescent product of H2DCF-DA, and a laser scanning confocal microscope (MRC1024ES, Biorad, Maylands, UK) with 488-nm excitation and 510-nm emission filters were used to monitor the generation of ROS in neurons treated with 10μM Aβ (25-35) for 24h. Glutamate secreted into the incubation medium for 6h from 10μM Aβ (25-35) treated cells was quantified by a high per- formance liquid chromatography (HPLC) with an electro- chemical detector (ECD) (MF series, BAS, IN, USA).
Retention trial was given 24h after the acquisition trial. To discard the possible effects of Aβ (25-35) on motor function, the animals were subjected to an activity monitor, a photobeam monitoring system (AM1051, Benwick Electronics, Benwick, UK), and rota-rod apparatus (Daejong Inc., Seoul, Korea) to examine locomotor activity and motor coordination, respectively. Each mouse was placed in the center of the activity cage, and the total number of mobile count was registered for 5 min and then put on the rota-rod for 2min.
대상 데이터
Louis, MO, USA). Hoechst 33342 dye, Fluo-4 AM and 2', 7'-dichlorodihydrofluorescin diacetate (H2DCF-DA) were purchased from Molecular Probes Inc. (Eugene, OR, USA). Fetal bovine serum was purchased from Gibco (Logan, UT, USA).
6×250mm, 5μm, Eclipse XDB-C18, Agilent, CA, USA). It was identified as homo-flavoyadorinin B, by comparing its retention time and UV pattern with those of authentic sample (Fig. 1). Authentic homoflavoyadorinin B was obtained from GHAM Bio- Pharm, Daegu, Korea.
데이터처리
Data were expressed as the mean ±S.E.M., and statistical significance was assessed by one- way analysis of variance (ANOVA) and Tukey’s tests. P<0.
이론/모형
Inhibitory effect of KM on Aβ (25-35)-induced cell death in cultured cortical neurons. Neuronal death was measured using the MTT assay. The MTT absorbance from non-treated cells was normalized to 100%.
성능/효과
37 These results suggest evidences of the possibility of KM having neuroprotective effect in AD brains with the prevention of the disease progression. In conclusion, the present study provides a mechanistic explanation that KM has protective effect against Aβ (25-35)-induced neuronal cell death and memory impairment. The protection against Aβ (25-35)-induced neurotoxicity by KM may provide the pharmacological basis of its therapeutic promise in prevention of neurodegeneration in AD.
measured in mice. The results showed that both KM and Aβ (25-35) did not significantly affect locomotor and rota-rod activity (Table 1). These results indicate that KM as well as Aβ (25-35) has no effect on general motor function and the improvement of memory was not associated with immobility, which might be caused by KM administration.
The results showed that both KM and Aβ (25-35) did not significantly affect locomotor and rota-rod activity (Table 1). These results indicate that KM as well as Aβ (25-35) has no effect on general motor function and the improvement of memory was not associated with immobility, which might be caused by KM administration.
후속연구
33 The protection by KM against Aβ (25-35)-induced memory deficit was not due to possibly caused immobility as KM did not affect general motor function in mice. Further studies should be performed to clarify the mechanism.
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