Neuroprotective effects of exogenous activin A on oxygen-glucose deprivation in PC12 cells.

Neuroprotective effects of exogenous activin A on oxygen-glucose deprivation in PC12 cells.
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DOI:
10.3390/molecules17010315
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发表时间:
2011-12-30
期刊:
Molecules (Basel, Switzerland)
影响因子:
--
通讯作者:
Xu ZX
Xu ZX
中科院分区:
其他
文献类型:
--
作者:
He JT;Mang J;Mei CL;Yang L;Wang JQ;Xing Y;Yang H;Xu ZX

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缺血性脑血管病是世界上最常见的死亡原因之一。外源性激活素A(ActA)保护神经元免受毒性,并在调节大脑对损伤的反应中发挥重要作用。在本研究中,我们研究了ActA在缺氧缺血性脑疾病模型中的神经保护作用的机制。我们发现ActA能有效地提高PC 12细胞的存活率,减轻氧糖剥夺(OGD)损伤。为阐明ActA的神经保护机制,本研究采用OGD法观察ActA对PC 12细胞ActA/Smad通路的影响以及对诱导型一氧化氮合酶(NOS)和超氧化物歧化酶(SOD)表达的影响。结果表明,ActA可增加激活素受体IIA(ActRIIA)、Smad 3和Smad 4的表达,50 ng/mL和100 ng/mL的ActA可使NO水平降低78.9%和SOD活性提高79.9%。提示ActA的神经保护作用可能与其激活ActA/Smad信号通路及抗氧化活性有关。
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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