Polychlorinated biphenyls (PCBs) are persistent pollutants involved in human tumorigenesis. PCB153 is a ubiquitous non-dioxin-like PCB with proliferative and anti-apoptotic effects. To explore the impact of PCB153 in the survival of pituitary cells, we exposed murine pituitary primary cells to PCB153 10 μM for 24h. Apoptosis was assessed by RT-qPCR, Western-blot, immunoprecipitation, caspase activity, and immunofluorescence. We found that PCB153 decreased pituitary apoptosis through both the extrinsic and intrinsic pathways. PCB153 reduced the level of the pro-apoptotic protein p38-MAPK. Otherwise, PCB153 activated PI3K/Akt and Erk1/2 pathways and enhanced the expression and nuclear translocation of NF-κB. Cotreatments with specific inhibitors revealed that only PI3K/Akt changed the caspase-3 expression and NF-κB activation induced by PCB153. Also, PCB153 decreased the expression of the pro-apoptotic and pro-senescent cyclins p53 and p21. In summary, exposure to PCB153 leads to a downregulation of apoptosis in the pituitary driven by a PI3K/Akt-mediated activation of NF-κB.

多氯联苯（PCB）是与人类肿瘤发生有关的持久性污染物。 PCB153是一种普遍存在的非二恶英类PCB，具有增殖和抗凋亡作用。为了探讨 PCB153 对垂体细胞存活的影响，我们将小鼠垂体原代细胞暴露于 10 μM PCB153 中 24 小时。通过 RT-qPCR、Western-blot、免疫沉淀、半胱天冬酶活性和免疫荧光评估细胞凋亡。我们发现 PCB153 通过外在和内在途径减少垂体细胞凋亡。 PCB153 降低促凋亡蛋白 p38-MAPK 的水平。另外，PCB153 激活 PI3K/Akt 和 Erk1/2 通路并增强 NF-κB 的表达和核转位。与特定抑制剂的共同治疗表明，只有 PI3K/Akt 改变了 PCB153 诱导的 caspase-3 表达和 NF-κB 激活。此外，PCB153 还降低了促凋亡和促衰老细胞周期蛋白 p53 和 p21 的表达。总之，暴露于 PCB153 会导致垂体中由 PI3K/Akt 介导的 NF-κB 激活驱动的细胞凋亡下调。