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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Prosurvival role of JAK/STAT and Akt signaling pathways in MPP+-induced apoptosis in neurons.
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Prosurvival role of JAK/STAT and Akt signaling pathways in MPP+-induced apoptosis in neurons.

机译：JAK / STAT和Akt信号通路在MPP +诱导的神经元凋亡中的生存作用。

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摘要

In the present study the role of JAK/STAT and Akt in apoptosis was evaluated in cerebellar granule cells after treatment with the mitochondrial toxin MPP(+). Firstly, we evaluated the role of the prosurvival Akt pathway in MPP(+)-induced apoptosis and found that MPP(+) rapidly reduced the phosphorylation of Akt at Ser473. Since PTEN is an upstream regulator of Akt, its inhibition with bpV(pic) (1-30 muM) should activate Akt, however, it did not attenuate CGC cell death mediated by MPP(+) but protected CGC from apoptosis mediated by S/K deprivation. We also demonstrated that after the treatment with the complex I inhibitor, the expression levels of STAT1 increased and the levels of STAT3 decreased at the time points tested (0.5-8h). Meanwhile, pharmacological inhibition of the JAK/STAT pathway with AG490 (10-40 muM) was neuroprotective, probably due to its antioxidant properties, the Jak2-inhibitor-II potentiated MPP(+) neurotoxicity. Collectively, our data indicate that the treatment of CGC with the neurotoxin MPP(+) decreased two prosurvival pathways: STAT3 and Akt. Meanwhile Akt activation, using a PTEN inhibitor, did not play a prominent role in neuroprotection; loss of STAT3 could be a signal pathway involved in neuroprotection against the Parkinsonian neurotoxin MPP(+).
机译：在本研究中，用线粒体毒素MPP（+）处理后，在小脑颗粒细胞中评估了JAK / STAT和Akt在凋亡中的作用。首先，我们评估了生存Akt途径在MPP（+）诱导的细胞凋亡中的作用，发现MPP（+）迅速减少了Ser473上Akt的磷酸化。由于PTEN是Akt的上游调节剂，因此其对bpV（pic）（1-30 muM）的抑制作用应激活Akt，但是，它不能减弱MPP（+）介导的CGC细胞死亡，但可以保护CGC免受S /介导的细胞凋亡。 K剥夺。我们还证明了在用复合物I抑制剂治疗后，在测试的时间点（0.5-8h）STAT1的表达水平增加而STAT3的水平下降。同时，AG490（10-40μM）对JAK / STAT途径的药理抑制作用具有神经保护作用，这可能是由于其抗氧化特性，Jak2-inhibitor-II增强了MPP（+）的神经毒性。总的来说，我们的数据表明，神经毒素MPP（+）对CGC的治疗降低了两种生存途径：STAT3和Akt。同时，使用PTEN抑制剂的Akt激活在神经保护中没有发挥重要作用。 STAT3的丢失可能是参与针对帕金森氏神经毒素MPP（+）的神经保护的信号途径。

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