| 易梦妮,韦天娇,陆 琴,高小玲,虞志华.KCa3.1通道参与调控星形胶质细胞糖氧剥夺诱导的内质网应激[J].,2017,17(30):5801-5806 |
| KCa3.1通道参与调控星形胶质细胞糖氧剥夺诱导的内质网应激 |
| KCa3.1 Channel was involved in the Regulation of Oxygen and Glucose Deprivation - induced Endoplasmic Reticulum Stress in Astrocytes |
| 投稿时间：2017-05-23 修订日期：2017-06-20 |
| DOI：10.13241/j.cnki.pmb.2017.30.001 |
| 中文关键词: KCa3.1 OGD 星形胶质细胞 内质网应激 |
| 英文关键词: KCa3.1 OGD Astrocytes Endoplasmic reticulum stress |
| 基金项目:国家自然科学基金项目（81373351）；上海市自然科学基金项目（16ZR1418700） |
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| 中文摘要: |
| 摘要 目的：研究KCa3.1在糖氧剥夺诱导的原代星形胶质细胞内质网应激（ERS）中的调控作用。方法：通过构建原代星形胶质细胞糖氧剥夺（OGD）模型，应用cck-8法、免疫荧光技术、western blotting等分子生物学技术研究KCa3.1在OGD引起的原代星形胶质细胞内质网应激中的作用。结果：OGD 4 h处理后星形胶质细胞内KCa3.1的表达明显上调。OGD处理后星形胶质细胞的细胞活力显著性降低，且具有时间依赖性。给予KCa3.1通道抑制剂TRAM-34可提高OGD 4 h处理后星形胶质细胞的细胞活力，并具有剂量依赖性。OGD处理0.5 h、1 h、3 h、4 h、6 h后，原代星形胶质细胞内ERS信号通路被激活，GRP78、p-eIF-2α的表达显著性上调。给予KCa3.1通道抑制剂TRAM-34后，OGD引起的星形胶质细胞内GRP78、p-eIF-2α的上调幅度显著性降低。结论：KCa3.1通道参与了星形胶质细胞内OGD引起的内质网应激通路的激活。 |
| 英文摘要: |
| ABSTRACT Objective: To evaluate the regulation of KCa3.1 in oxygen and glucose deprivation-induced endoplasmic reticulum stress in primary astrocytes. Methods: The model of oxygen and glucose deprivation in primary astrocytes were constructed to explore the role of Ka3.1 channel on OGD-induced endoplasmic reticulum stress by using cell biology and molecular biology techniques including cck-8, immunofluorescence technique and western blotting. Results: Expression of KCa3.1 protein in astrocytes subjected to OGD 4 h was significantly up-regulated. Cell viability of astrocytes subjected to OGD was significantly time-dependent lower. KCa3.1 channel inhibitor, TRAM-34, could improve the cell viability of astrocytes treated with OGD 4 h, which was dose-dependent. ERS signaling pathway was activated in primary astrocytes at 0.5 h, 1 h, 3 h, 4 h, 6 h after OGD. The expression of GRP78 and p-eIF-2α protein was significantly up-regulated. The up-regulation of GRP78 and p-eIF-2α in the TRAM-34 group after OGD treatment was significantly inhibited. Conclusion: KCa3.1 channel is involved in the activation of endoplasmic reticulum stress pathway induced by OGD in primary astrocytes. |
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