Modulation of astrocytic glutamine synthetase expression and cell viability by histamine in cultured cortical astrocytes exposed to OGD insults
Modulation of astrocytic glutamine synthetase expression and cell viability by histamine in cultured cortical astrocytes exposed to OGD insults
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组胺对暴露于 OGD 损伤的培养皮质星形胶质细胞中星形胶质细胞谷氨酰胺合成酶表达和细胞活力的调节
DOI：
10.1016/j.neulet.2013.06.013
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发表时间：
2013-08
影响因子：
2.5
通讯作者：
Zhong Chen
中科院分区：
文献类型：
--
作者：
Hai-jing Yan;Li Tan;Jie-qiong Gao;Yue-yang Tian;Xiao-jie Shi;Wei-wei Hou;Juan Li;Yao Shen;Zhong Chen
组胺是一种神经递质或神经调质，已被证明在脑缺血中具有神经保护作用。然而，关于其在脑缺血时对星形胶质细胞的作用的报道很少。本研究的目的是探讨组胺对原代培养的皮质星形胶质细胞氧糖剥夺（OGD）损伤后星形胶质细胞损伤和谷氨酸信号传导的影响，特别是对谷氨酰胺合成酶（GS）表达的影响。OGD 6 h可导致星形胶质细胞线粒体功能严重受损，GS表达降低，细胞外谷氨酸水平升高。组胺预处理可明显抑制细胞损伤，并以浓度依赖性方式恢复GS的表达。组胺对星形胶质细胞损伤的保护作用可被H1受体拮抗剂吡拉明或H2受体拮抗剂西咪替丁部分逆转。然而，组胺对GS表达的调节作用仅被吡拉明拮抗。此外，双吲哚马来酰亚胺II，一种广谱的PKC抑制剂，逆转了组胺对GS表达的调节作用。提示组胺通过H1和H2受体对OGD诱导的星形胶质细胞损伤具有保护作用，其对星形胶质细胞GS表达的调节作用可能是通过激活H1受体和PKC途径实现的。组胺可能是一种内源性保护因子，并呼吁进一步研究其作为缺血性卒中星形胶质细胞功能的调节剂。
Histamine, a neurotransmitter or neuromodulator has been demonstrated to be neuroprotective in cerebral ischemia. However, few reports concern its function on astrocytes during cerebral ischemia. The purpose of this study was to investigate the effects of histamine on astrocytic cell damage and glutamate signaling, especially on glutamine synthetase (GS) expression in primary cultured cortical astrocytes exposed to oxygen-glucose deprivation (OGD) insult. OGD for 6 h caused a severe damage of astrocytic mitochondrial function, and decreased GS expression and then increased the extracellular glutamate level. Pretreatment with histamine significantly prevented the cell damage and rescued the expression of GS in a concentration-dependent manner. The protective effect of histamine on astrocytic cell damage could be partly reversed either by H1receptor antagonist pyrilamine or H2receptor antagonist cimetidine. However, the regulatory effect of histamine on GS expression was antagonized only by pyrilamine. In addition, bisindolylmaleimide II, a broad-spectrum inhibitor of PKC, reversed the regulatory action of histamine on GS expression. These results indicate that histamine can effectively protect against OGD-induced cell damage in astrocytes through H1and H2receptors, and its regulatory effect on astrocytic GS expression may be due to the activation of H1receptor and PKC pathway. Histamine may be an endogenous protective factor and calls for its further study as a regulator of astrocyte function during ischemic stroke.
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影响因子：
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作者：
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