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

被引：19

作者：

Guo, Hongliang ^{[1
,2
]}

Shen, Xiaoran ^{[3
]}

Xu, Ye ^{[4
]}

Yuan, Junliang ^{[1
]}

Zhao, Dongming ^{[2
]}

Hui, Wenli ^{[1
]}

机构：

[1] Capital Med Univ, Beijing Chaoyang Hosp, Dept Neurol, Beijing 100020, Peoples R China

[2] Beihua Univ, Jilin 132001, Jilin Province, Peoples R China

[3] Jilin Municipal Cent Hosp, Jilin 132001, Jilin Province, Peoples R China

[4] Jilin Med Coll, Jilin 132001, Jilin Province, Peoples R China

来源：

NEURAL REGENERATION RESEARCH | 2013年 / 8卷 / 15期

基金：

中国国家自然科学基金;

关键词：

neural regeneration; traditional Chinese medicine; emodin; oxygen-glucose deprivation; activin A; apoptosis; caspase-3; neuroprotection; grants-supported paper; neuroregeneration; IN-VITRO; TGF-BETA; APOPTOSIS; TARGET; CANCER; GROWTH; BRAIN; CELLS; VIVO;

D O I：

10.3969/j.issn.1673-5374.2013.15.002

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

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.

引用

页码：1360 / 1367

页数：8