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Involvement of ERK and CREB Signaling Pathways in the Protective Effect of PACAP in Monosodium Glutamate-Induced Retinal Lesion

机译:ERK和CREB信号传导途径参与PAPAP在谷氨酸钠诱导的视网膜病变中的保护作用

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Pituitary adenylate cyclase-activiting poly peptide (PACAP) has well-documented neuroprotective actions, which have also been shown in retinal degeneration induced by monosodium glutamate (MSG) in neonatal rats. The aim of this article was to investigate the activation of extracellular signal-regulated kinase (ERK1/2) and cyclic adenosine 3',5'-phosphate (cAM P)-responsive element binding protein (CREB) signaling pathways by Western blot analysis in retinal degeneration induced by MSG. We found that intravitreal administration of PACAP preceding the MSG treatments induced significant increases in the phosphorylation, that is, the activation of ERK1/2 and its downstream target, CREB, 12 h after the treatment compared to the contralateral untreated eye during the first two treatments, with no further elevations 24 h after treatments. These results demonstrate that the degenerative effect of MSG and the protective effect of PACAP involve complex kinase signaling pathways and are related to CAMP/ERK/CREB activation.
机译:垂体腺苷酸环化酶activiting聚肽(PACAP)已充分证明神经保护作用,这也已在由新生大鼠谷氨酸一钠(MSG)诱导的视网膜变性所示。本文的目的是调查细胞外信号调节激酶的活化(ERK1 / 2)和环腺苷3' ,5'-磷酸(CAM P)响应性元件结合蛋白(CREB)通过Western印迹分析信号转导途径视网膜变性味精所致。我们发现PACAP诱导的磷酸化,即,ERK1 / 2和其下游靶标,CREB,相比对侧未经处理的眼的治疗前两个处理过程中后12小时的活化显著增加MSG治疗前该玻璃体内给药的,没有进一步升高处理后24个小时。这些结果表明,MSG的退行性效果和PACAP的保护作用涉及复杂的激酶信号传导途径和相关的CAMP / ERK / CREB激活。

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