Protective effect of the aerial parts of Silybum marianum against amyloid β protein (25-35)-induced neuronal death in cultured neurons
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서지정보
ㆍ발행기관 : 충북대학교 동물의학연구소
ㆍ수록지정보 : Journal of Biomedical and Translational Research / 17권 / 4호
ㆍ저자명 : Hae Min Lee, Ji Yeon Jang, Yeon Hee Seong
ㆍ저자명 : Hae Min Lee, Ji Yeon Jang, Yeon Hee Seong
목차
IntroductionMaterials and Methods
Plant materials and extraction and reagents
Experimental animals
Induction of neurotoxicity and analysis of neuronalviability in primary cultures of rat cerebral corticalneurons
Western blotting
Statistical analysis
Results
Protective effect of SM against Aβ (25-35)-inducedneuronal cell death
Inhibitory effect of SM on Aβ-induced change ofapoptosis-associated proteins
Protective effect of SM against NMDA-inducedneuronal cell death
Discussion
References
영어 초록
Alzheimer’s disease (AD), a progressive neurodegenerative disorder that deprives the patient of memory, is associated mainly with extracellular senile plaque induced by the accumulation of amyloid β protein (Aβ). Silybum marianum (Asteraceae; SM) is a medicinal plant that has long been used in traditional medicine as a hepatoprotective remedy owing to its antioxidant and anti-inflammatory activities. The present study examined the methanol extract of the aerial parts of SM for neuroprotection against Aβ (25-35)-induced neuronal death in cultured rat cortical neurons to investigate a possible therapeutic role of SM in AD. The primary cortical neuron cultures were prepared using embryonic day 15 to 16 SD rat fetuses. Cultured cortical neurons exposed to 10 μM Aβ (25-35) for 36 h underwent neuronal cell death. At 10 and 50 μg/mL, SM prevented Aβ (25-35)-induced neuronal cell death and apoptosis in cultured cortical neurons. Furthermore, SM inhibited the Aβ (25-35)-induced decrease in anti-apoptotic protein, Bcl-2, and the increase in the proapoptotic proteins, Bax and active caspase-3. Cultured cortical neurons exposed to 1 mM N-methyl-D-aspartate (NMDA) for 14 h induced neuronal cell death. SM (10 and 50 μg/mL) prevented NMDA-induced neuronal cell death. These results suggest that SM inhibited Aβ (25-35)-induced neuronal apoptotic death via inhibition of NMDA receptor activation and that SM has a possible therapeutic role in preventing the progression of neurodegeneration in AD.참고 자료
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