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目的:通过离体培养脊髓星形胶质细胞,探讨谷氨酸对缝隙连接蛋白43磷酸化的调节机制。方法:实验分为正常对照组、谷氨酸刺激组(10μmol/L谷氨酸作用24 h)、PKC抑制剂组(20μmol/L Go6976作用24 h)。Western Blot法检测各组星形胶质细胞中P-CX43、P-PKC、P-ERK蛋白的表达;细胞免疫荧光法检测各组星形胶质细胞P-CX43胞膜蛋白的表达。结果:谷氨酸刺激组与正常对照组相比,星形胶质细胞P-CX43、P-PKC蛋白的表达增加(P<0.05);在谷氨酸刺激的基础上给予PKC抑制剂作用后P-CX43的表达降低(P<0.05)。结论:谷氨酸可以通过PKC通路使CX43的磷酸化增加。
OBJECTIVE: To investigate the regulatory mechanism of glutamate on the phosphorylation of connexin43 by in vitro culture of spinal cord astrocytes. Methods: The experiment was divided into normal control group, glutamate stimulation group (10μmol / L glutamate for 24 h), PKC inhibitor group (20μmol / L Go6976 for 24 h). The expression of P-CX43, P-PKC and P-ERK in astrocytes were detected by Western Blot. The expression of P-CX43 protein in astrocytes was detected by immunofluorescence. Results: Compared with the normal control group, the expression of P-CX43 and P-PKC in astrocyte increased (P <0.05), and the effect of PKC inhibitor on the basis of glutamate stimulation The expression of P-CX43 was decreased (P <0.05). CONCLUSION: Glutamate increases CX43 phosphorylation through the PKC pathway.