Fluoxetine Up-Regulates Bd-xL Expression in Rat C6 Glioma Cells
Fluoxetine Up-Regulates Bd-xL Expression in Rat C6 Glioma Cells
复制标题
DOI：
10.4306/pi.2011.8.2.161
复制
发表时间：
2011-06-01
影响因子：
2.7
通讯作者：
Park, Yong-Chon
中科院分区：
文献类型：
--
作者：
Choi, Mi Ran;Oh, Dong Hoon;Park, Yong-Chon
目的探讨氟西汀对大鼠C6胶质瘤细胞急性和慢性作用后的差异表达基因及Bcl-xL蛋白表达的影响。结果基因芯片检测结果显示，氟西汀作用24 h后，Bcl-xL和NCAM 140等33个基因表达上调，cyclin G相关激酶等7个基因表达下调。氟西汀处理72 h后，上调53个基因（包括Gs α和Bcl-xL），下调77个基因（包括Gai 2和annexin V）。基于qRT-PCR结果，与对照相比，在氟西汀处理的细胞中，在72小时时Gsa mRNA增加，G α 12 mRNA减少，该结果与微阵列一致。我们还观察到增加Bcl-xL mRNA（无论是在24小时和72小时）在氟西汀处理的细胞相比，控制，表现出逐渐增加的趋势。结论氟西汀长期治疗不仅通过诱导Gsa表达启动cAMP通路，而且通过诱导Bcl-xL表达，从而抑制细胞凋亡。精神病学调查2011;8：161-168
Objective To analyze both differentially expressed genes and the Bcl-xL protein expression after acute and chronic treatment with fluoxetine in rat C6 glioma cells.Methods C6 glioma cells were cultured for 24 h or 72 h after treatment with 10 mu M fluoxetine, and gene expression patterns were observed using microarray and qRT-PCR. Then, cells were cultured for 6 h, 24 h, 72 h or 96 h after treatment with 10 mu M fluoxetine, and the expression of Bd-xL protein was measured using western blot.Results As determined by microarray, treatment with fluoxetine for 24 h up-regulated 33 genes (including Bcl-xL and NCAM140) and down-regulated 7 genes (including cyclin G-associated kinase). Treatment with fluoxetine for 72 h up-regulated 53 genes (including Gs alpha and Bcl-xL) and down-regulated 77 genes (including Gai2 and annexin V). Based on the qRT-PCR results, there was an increase in Gsa mRNA and a decrease in G alpha i2 mRNA at 72 h in fluoxetine-treated cells as compared to control, a result that was consistent with microarray. We also observed an increase in Bcl-xL mRNA (both at 24 h and at 72 h) in fluoxetine-treated cells as compared to control, demonstrating a tendency to increase gradually. Bcl-xL protein expression increased as the duration of fluoxetine treatment increased.Conclusion These results suggest that chronic treatment with fluoxetine not only initiates the cAMP pathway through inducing Gsa expression but also induces Bcl-xL expression, thus inhibiting apoptosis. Psychiatry Investig 2011;8:161-168