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

• Published in: Neural regeneration research 2013-05, Vol.8 (15), p.1360-1367
• Main Authors: Guo, Hongliang, Shen, Xiaoran, Xu, Ye, Yuan, Junliang, Zhao, Dongming, Hu, Wenli
• Format: Article
• Language: English
• Subjects: caspase-3; Research and Report : Traditional Chinese Medicine and Neural Regeneration; 大黄素; 激活素; 神经元损伤; 神经元样细胞; 神经生长因子; 缺氧缺血; 缺血性脑损伤
• ISSN: 1673-5374; 1876-7958
• DOI: 10.3969/j.issn.1673-5374.2013.15.002

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 shewed 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.