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。 AIM: To investigate the regulatory role of KCa3.1 in endoplasmic reticulum stress (ERS) induced by glucose-oxygen deprivation. Methods: The primary astrocytes were induced by OGD (Oxygen Deprivation-Deprivation) model (OGD), ckc-8 method, immunofluorescence technique, western blotting and other molecular biological techniques. Role of cells in endoplasmic reticulum stress. Results: The expression of KCa3.1 in astrocytes after OGD 4 h treatment was significantly up-regulated. The viability of astrocytes after OGD treatment decreased significantly and was time-dependent. Administration of KAM3.1 channel inhibitor TRAM-34 increased the viability of astrocytes after 4 h OGD treatment in a dose-dependent manner. After OGD treatment for 0.5 h, 1 h, 3 h, 4 h, and 6 h, the ERS signaling pathway in primary astrocytes was activated, and the expressions of GRP78 and p-eIF-2α were significantly up-regulated. After administration of KAM3.1 channel inhibitor TRAM-34, the upregulation of GRP78 and p-eIF-2α in astrocytes induced by OGD decreased significantly. Conclusion: KCa3.1 channel is involved in the activation of endoplasmic reticulum stress pathway induced by OGD in astrocytes.