Yubin Liang1, Min Huang2, Xin Jiang3, Qiong Liu4, Xin Chang1, Yi Guo5. 1. Department of Neurology, 2nd Clinical Medical College of Jinan University, Shenzhen, Guangdong, China. 2. Department of Neurology, 2nd Clinical Medical College of Jinan University, Shenzhen, Guangdong, China; Department of Neurology, the seventh Affiliated Hospital, Sun Yat-sen University, Shenzhen, Guangdong, China. 3. Department of Geriatrics, 2nd Clinical Medical College of Jinan University, Shenzhen, Guangdong, China. 4. College of Life Sciences, Shenzhen University, Shenzhen, China. 5. Department of Neurology, 2nd Clinical Medical College of Jinan University, Shenzhen, Guangdong, China. Electronic address: xuanyi_guo@163.com.
Abstract
BACKGROUND AND PURPOSE: Neuronal cell apoptosis is an important pathological change in Alzheimer's disease (AD). Berberine, an isoquinoline alkaloid isolated and extracted from Coptidis and rhizome and Cortex phellodendri, has a wide range of pharmacological effects. In this study, we investigated the neuroprotective effects of Berberine against neuronal insults induced by Aβ25-35 in primary cultured hippocampal neurons. METHODS: Primary neuron cells have been isolated from hippocampus of C57BL/6 newborn mice. We investigated effect of Berberine against neuronal insults induced by Aβ25-35 in primary cultured hippocampal neurons. TdT-mediated dUTP nick-end labeling, MTT, Propidium iodide, MMP, Caspase activity measurement, Western blot. RESULT: These neurons explosure to the β25-35 protein resulted in a loss in cell viability and a surge in apoptosis. However, the presence of Berberine significantly reversed the effects induced by Aβ25-35. Through decreasing viability and caspase activity in neurons, the pretreatment with Berberine attenuated the cytotoxic effect of the Aβ25-35. Furthermore, it's found that expression of cytochrome C, as well as the restoration of Bcl-2/Bax and Bcl-xl/Bax ratio in the presence of Berberine, led to a decline in the apoptotic rate. CONCLUSION: The neuroprotective effects of Berberine against Aβ25-35-induced neuronal apoptosis, suggesting that this may be a promising therapeutics against AD.
BACKGROUND AND PURPOSE: Neuronal cell apoptosis is an important pathological change in Alzheimer's disease (AD). Berberine, an isoquinoline alkaloid isolated and extracted from Coptidis and rhizome and Cortex phellodendri, has a wide range of pharmacological effects. In this study, we investigated the neuroprotective effects of Berberine against neuronal insults induced by Aβ25-35 in primary cultured hippocampal neurons. METHODS: Primary neuron cells have been isolated from hippocampus of C57BL/6 newborn mice. We investigated effect of Berberine against neuronal insults induced by Aβ25-35 in primary cultured hippocampal neurons. TdT-mediated dUTP nick-end labeling, MTT, Propidium iodide, MMP, Caspase activity measurement, Western blot. RESULT: These neurons explosure to the β25-35 protein resulted in a loss in cell viability and a surge in apoptosis. However, the presence of Berberine significantly reversed the effects induced by Aβ25-35. Through decreasing viability and caspase activity in neurons, the pretreatment with Berberine attenuated the cytotoxic effect of the Aβ25-35. Furthermore, it's found that expression of cytochrome C, as well as the restoration of Bcl-2/Bax and Bcl-xl/Bax ratio in the presence of Berberine, led to a decline in the apoptotic rate. CONCLUSION: The neuroprotective effects of Berberine against Aβ25-35-induced neuronal apoptosis, suggesting that this may be a promising therapeutics against AD.