BMC Anesthesiol：右美托咪定或可有效治疗脑缺血损伤

2017-09-05 MedSci MedSci原创

本研究旨在探讨在PC12细胞和原代神经元细胞中右美托咪定（DMED）对缺氧缺糖（OGD）所诱导的脑损伤。研究人员将PC12细胞暴露于OGD以建立缺血模型。使用细胞存活率、凋亡相关蛋白的表达和凋亡来评估OGD诱导的细胞损伤。OGD和DMED治疗后探究氧化应激和神经营养因子的表达。OGD和DMED治疗后探究可能涉及的信号通路，并随后加入抑制剂抑制通路。最后，根据炎症因子和氧化应激的变化研究DMED对初

本研究旨在探讨在PC12细胞和原代神经元细胞中右美托咪定（DMED）对缺氧缺糖（OGD）所诱导的脑损伤。

研究人员将PC12细胞暴露于OGD以建立缺血模型。使用细胞存活率、凋亡相关蛋白的表达和凋亡来评估OGD诱导的细胞损伤。OGD和DMED治疗后探究氧化应激和神经营养因子的表达。OGD和DMED治疗后探究可能涉及的信号通路，并随后加入抑制剂抑制通路。最后，根据炎症因子和氧化应激的变化研究DMED对初级神经元细胞的作用。

结果显示，在OGD诱导的PC12细胞中，DMED可明显增加细胞活力，并细胞凋亡减少，以及Bax/Bcl-2的比值。然后，OGD诱导的LDH、MDA、SOD、GSH-Px活性以及神经营养因子水平的减少均可由DMED治疗改善。OGD处理后NF-κB信号通路的关键激酶上调，而DMED处理后则降低。此外，Notch或NF-κB抑制剂或可增加DMED对OGD诱导的细胞损伤的影响。最后，研究人员确定了DMED对原代神经元细胞的保护作用。

总之， DMED对OGD诱导的PC12细胞损伤具有保护作用，取决于其抗凋亡、抗氧化活性以及对NF-κB活化的抑制。该研究结果表明，DMED可作为脑缺血的潜在治疗药物。

原始出处：

Ya-Jun Liu, Duan-Yu Wang, et al., Effects and mechanism of dexmedetomidine on neuronal cell injury induced by hypoxia-ischemia. BMC Anesthesiol. 2017; 17: 117. Published online 2017 Aug 30. doi: 10.1186/s12871-017-0413-4.

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2018-04-17 ms3025846204744509

#BMC#

20 0
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2018-02-11 智慧医人

#脑缺血损伤#

0 0
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2018-08-04 xiangyuzhou971

#EST#

27 0
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2017-09-07 cqlidoudou

#脑缺血#

25 0
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2017-09-07 ms3046638856685384

#损伤#

29 0
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2017-09-07 一叶知秋

#ESI#

21 0
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2017-09-07 docwu2019

#有效治疗#

23 0
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2017-09-06 一个字-牛

学习了谢谢分享

53 0
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2017-09-05 1e0f8808m18(暂无匿称)

脑缺血损伤治疗或又多一药物

54 0

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