Emodin prevents hypoxic-ischemic neuronal injury Involvement of the activin A pathway |
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| Authors: | Hongliang Guo Xiaoran Shen Ye Xu Junliang Yuan Dongming Zhao Wenli Hu |
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| Affiliation: | Hongliang Guo (Department of Neurology, Beijing Chaoyang Hospital Affiliated to Capital Medical University, Beijing 100020, China;Beihua University, Jilin 132001, Jilin Province, China); Xiaoran Shen (Jilin Municipal Central Hospital, Jilin 132001, Jilin Province, China); Ye Xu (Jilin Medical College, Jilin 132001, Jilin Province, China); Junliang Yuan (Department of Neurology, Beijing Chaoyang Hospital Affiliated to Capital Medical University, Beijing 100020, China); Dongming Zhao (Beihua University, Jilin 132001, Jilin Province, China); Wenli Hu (Department of Neurology, Beijing Chaoyang Hospital Affiliated to Capital Medical University, Beijing 100020, China); |
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| Abstract: | Emodin, an extract of dried rhizomes and the root of the Rhizoma Polygoni Cuspidati, can protect neurons from hypoxic-ischemic brain damage. This study aimed to verify the underlying mechanism. After PC12 cells had differentiated into neuron-like cells under the induction of mouse nerve growth factor, cells were subjected to oxygen-glucose deprivation and treated with emodin. Results showed that the viability of neuron-like cells cultured under an ischemia-hypoxia environment decreased, while the expression of activin A and caspase-3 in cells increased. Emodin raised the survival rate of oxygen-glucose deprived neuron-like cells, increased activin A expression, and decreased caspase-3 expression. Experimental findings indicate that emodin can inhibit neuronal apoptosis and alleviate the injury of nerve cells after oxygen-glucose deprivation through the activin A pathway. |
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| Keywords: | neural regeneration traditional Chinese medicine emodin oxygen-glucose deprivation activin A apoptosis caspase-3 neuroprotection grants-supported paper neuroregeneration |
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