Xin Qiu1, Guo-hua Chen, Tao Wang. 1. Department of Neurology, Wuhan Hospital of Integrated Traditional and Western Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan.
Abstract
OBJECTIVE: To observe the effects of Huanglian Jiedu Decoction (HLJDT) on the metabolism of free radicals, the morphology and histopathology of hippocampal CA1 neurons in PS1/APP double transgenic mice of Alzheimer's disease (AD), and to study its possible mechanisms, thus providing experimental evidence for treating AD by HLJDT. METHODS: The APP/PS1 double transgenic mouse model was used. Mice were randomly divided into five groups, i. e., the model control group, the positive control group (Aricept), high-, middle-, and low-dose HLJDT group (at the daily dose of 865 mg*kg(-1), 433 mg*kg(-1), and 216 mg*kg(-1), respectively). Corresponding medication was daily given by gastrogavage. Seven months later superoxide dismutase (SOD) and malondialdehyde (MDA) were detected at the ten-month old mice, thus observing the effects on the morphology of CA1 hippocampal neurons and the senile plaques (SP). RESULTS: HLJDT and Aricept could obviously increase the SOD contents and lower the MDA contents (P<0.05), attenuate the destroy of neurocytes and the formation of SP, effectively hinder the degeneration of hippocampal neurons. Better results were obtained in the middle-dose HLJDT group than in the positive control group (P<0.05). CONCLUSION: The mechanism of HLJDT in treating AD might be possibly correlated with improving anti-oxygenation, protecting hippocampal neurocytes, and reducing the formation of SP.
OBJECTIVE: To observe the effects of Huanglian Jiedu Decoction (HLJDT) on the metabolism of free radicals, the morphology and histopathology of hippocampal CA1 neurons in PS1/APP double transgenic mice of Alzheimer's disease (AD), and to study its possible mechanisms, thus providing experimental evidence for treating AD by HLJDT. METHODS: The APP/PS1 double transgenicmouse model was used. Mice were randomly divided into five groups, i. e., the model control group, the positive control group (Aricept), high-, middle-, and low-dose HLJDT group (at the daily dose of 865 mg*kg(-1), 433 mg*kg(-1), and 216 mg*kg(-1), respectively). Corresponding medication was daily given by gastrogavage. Seven months later superoxide dismutase (SOD) and malondialdehyde (MDA) were detected at the ten-month old mice, thus observing the effects on the morphology of CA1 hippocampal neurons and the senile plaques (SP). RESULTS: HLJDT and Aricept could obviously increase the SOD contents and lower the MDA contents (P<0.05), attenuate the destroy of neurocytes and the formation of SP, effectively hinder the degeneration of hippocampal neurons. Better results were obtained in the middle-dose HLJDT group than in the positive control group (P<0.05). CONCLUSION: The mechanism of HLJDT in treating AD might be possibly correlated with improving anti-oxygenation, protecting hippocampal neurocytes, and reducing the formation of SP.