알츠하이머병 생쥐모델에서 인삼과 생지황 추출물의 효과
Effects of Ginseng and Rehmanniae Radix Extracts on Alzheimer’s Mice
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This study evaluated the effects of Ginseng Radix and Rehmanniae Radix extracts on cognitive function and Alzheimer's disease(AD)-related biomarkers in APPswe/PSEN1dE9 transgenic mice. Behavioral testing, AChE activity assays, immunohistochemistry for β-amyloid, Tau protein, and CD68, as well as Western blot analyses, were performed. Ginseng Radix significantly improved cognitive performance in behavioral tests. Both Ginseng Radix and Rehmanniae Radix extracts reduced AChE activity, suggesting their potential to delay AD progression. Immunohistochemical analysis showed decreased β-amyloid and CD68 expression with Rehmanniae Radix, while combined treatment reduced Tau-protein levels. Western blot results further confirmed β-amyloid suppression by Ginseng Radix and Tau inhibition by the combined treatment. These findings suggest that Ginseng Radix may be more effective in enhancing cognitive function, while Rehmanniae Radix may play a greater role in modulating AD-related pathology.
Abstract
This study evaluated the effects of Ginseng Radix and Rehmanniae Radix extracts on cognitive function and Alzheimer's disease(AD)-related biomarkers in APPswe/PSEN1dE9 transgenic mice. Behavioral testing, AChE activity assays, immunohistochemistry for β-amyloid, Tau protein, and CD68, as well as Western blot analyses, were performed. Ginseng Radix significantly improved cognitive performance in behavioral tests. Both Ginseng Radix and Rehmanniae Radix extracts reduced AChE activity, suggesting their potential to delay AD progression. Immunohistochemical analysis showed decreased β-amyloid and CD68 expression with Rehmanniae Radix, while combined treatment reduced Tau-protein levels. Western blot results further confirmed β-amyloid suppression by Ginseng Radix and Tau inhibition by the combined treatment. These findings suggest that Ginseng Radix may be more effective in enhancing cognitive function, while Rehmanniae Radix may play a greater role in modulating AD-related pathology.