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Neural Regen Res. 2013 May 25;8(15):1360-7. doi: 10.3969/j.issn.1673-5374.2013.15.002.

Emodin prevents hypoxic-ischemic neuronal injury: Involvement of the activin A pathway.

Author information

1
Department of Neurology, Beijing Chaoyang Hospital Affiliated to Capital Medical University, Beijing 100020, China ; Beihua University, Jilin 132001, Jilin Province, China.
2
Jilin Municipal Central Hospital, Jilin 132001, Jilin Province, China.
3
Jilin Medical College, Jilin 132001, Jilin Province, China.
4
Department of Neurology, Beijing Chaoyang Hospital Affiliated to Capital Medical University, Beijing 100020, China.
5
Beihua University, Jilin 132001, Jilin Province, China.

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.

KEYWORDS:

activin A; apoptosis; caspase-3; emodin; grants-supported paper; neural regeneration; neuroprotection; neuroregeneration; oxygen-glucose deprivation; traditional Chinese medicine

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