Glycolaldehyde (GA) is a highly reactive hydroxyaldehyde and one of the glycolytic metabolites producing advanced glycation endproducts (AGEs), but its toxicity toward neurons and Schwann cells remains unclear. In the present study, we found that GA exhibited more potent toxicity than other AGE precursors (glyceraldehyde, glyoxal, methylglyoxal and 3-deoxyglucosone) against immortalized IFRS1 adult rat Schwann cells and ND7/23 neuroblastoma × neonatal rat dorsal root ganglion (DRG) neuron hybrid cells. GA affected adult rat DRG neurons and ND7/23 cells more severely than GA-derived AGEs, and exhibited concentration- and time-dependent toxicity toward ND7/23 cells (10 < 100 < 250 < 500 µM; 6 h < 24 h). Treatment with 500 µM GA significantly up-regulated the phosphorylation of c-jun N-terminal kinase (JNK) and p-38 mitogen-activated kinase (p-38 MAPK) in ND7/23 cells. Furthermore, GA-induced ND7/23 cell death was significantly inhibited due to co-treatment with 10 µM of the JNK inhibitor SP600125 or the p-38 MAPK inhibitor SB239063. These findings suggest the involvement of JNK and p-38 MAPK-signaling pathways in GA-induced neuronal cell death and that enhanced GA production under diabetic conditions might be involved in the pathogenesis of diabetic neuropathy.

中文翻译：

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乙醇醛通过激活c-Jun N端激酶和p-38 MAP激酶途径诱导感觉神经元死亡。

乙醇醛（GA）是一种高反应性羟醛，是产生高级糖基化终产物（AGEs）的糖酵解代谢产物之一，但其对神经元和雪旺细胞的毒性尚不清楚。在本研究中，我们发现GA对永生化的IFRS1成年大鼠雪旺细胞和ND7 / 23神经母细胞瘤×新生大鼠背根神经节（DRG）神经元具有比其他AGE前体（甘油醛，乙二醛，甲基乙二醛和3-脱氧葡糖酮）更强的毒性。杂种细胞。GA对成年大鼠DRG神经元和ND7 / 23细胞的影响要比GA衍生的AGEs更严重，并且对ND7 / 23细胞表现出浓度和时间依赖性的毒性（10 <100 <250 <500 µM； 6 h <24 h）。用500 µM GA处理可显着上调ND7 / 23细胞中c-jun N末端激酶（JNK）和p-38丝裂原活化激酶（p-38 MAPK）的磷酸化。此外，由于与10 µM JNK抑制剂SP600125或p-38 MAPK抑制剂SB239063共同处理，GA诱导的ND7 / 23细胞死亡被显着抑制。这些发现表明，JNK和p-38 MAPK信号通路参与了GA诱导的神经元细胞死亡，并且在糖尿病条件下增加的GA产量可能与糖尿病性神经病的发病机制有关。