Neuroprotective Effects of Exogenous Activin A on Oxygen-Glucose Deprivation in PC12 Cells

被引：30
作者：
He, Jin-Ting [1 ]
Mang, Jing [1 ]
Mei, Chun-Li [1 ,2 ]
Yang, Le [3 ]
Wang, Jiao-Qi [1 ]
Xing, Ying [1 ]
Yang, Hong [1 ]
Xu, Zhong-Xin [1 ]
机构：
[1] Jilin Univ, China Japan Friendship Hosp, Dept Neurol, Changchun 130012, Peoples R China
[2] Beihua Univ, Coll Nursing, Jilin 132013, Peoples R China
[3] Peoples Hosp Jilin Prov, Changchun 130021, Peoples R China
来源：
MOLECULES | 2012年 / 17卷 / 01期
关键词：
OGD; tolerance model; exogenous activin A; SIGNALING PATHWAY; ISCHEMIC-STROKE; RELEASE; OSTHOLE; STRESS; SYSTEM; ROLES; MODEL; SMAD; SKIN;
D O I：
10.3390/molecules17010315
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
Ischemic cerebrovascular disease is one of the most common causes of death in the World. Exogenous activin A (ActA) protects neurons against toxicity and plays a central role in regulating the brain's response to injury. In the present study, we investigated the mechanisms involved in the neuroprotective effects of ActA in a model of hypoxic-ischemic brain disease. We found that ActA could effectively increase the survival rate of PC12 cells and relieve oxygen-glucose deprivation (OGD) damage. To clarify the neuroprotective mechanisms of ActA, the effects of ActA on the ActA/Smad pathway and on the up-regulation of inducible nitric oxide synthase (NOS) and superoxide dismutase (SOD) were investigated using OGD in PC12 cells. The results showed that ActA could increase the expression of activin receptor IIA (ActRIIA), Smad3 and Smad4 and that 50 ng/mL and 100 ng/mL of ActA could reduce NO levels and increase SOD activity by 78.9% and 79.9%, respectively. These results suggested that the neuroprotective effects of ActA in ischemia could be related to the activation of the ActA/Smad signaling pathway and to its anti-oxidant activities.
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收藏
页码：315 / 327
页数：13
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