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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 >Hydrogen sulfide reduces mRNA and protein levels of beta-site amyloid precursor protein cleaving enzyme 1 in PC12 cells.
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Hydrogen sulfide reduces mRNA and protein levels of beta-site amyloid precursor protein cleaving enzyme 1 in PC12 cells.

机译：硫化氢可降低PC12细胞中β-位淀粉样蛋白前体蛋白裂解酶1的mRNA和蛋白水平。

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Hydrogen sulfide (H(2)S) is now identified as a new neuromodulator. Increasing evidence suggest that H(2)S may play an important role in the progression of Alzheimer's disease (AD). The aim of the present study is to investigate the effects of H(2)S on beta-site amyloid precursor protein cleaving enzyme 1 (BACE-1) expression and amyloid beta (Abeta) secretion in PC12 cells. The levels of BACE-1 mRNA were measured by quantitative polymerase chain reaction analysis. BACE-1 protein levels were assessed by Western blot. Cellular culture medium levels of Abeta1-42 were analyzed by ELISA. We found that sodium hydrosulfide (NaHS), a H(2)S donor, decreased BACE-1 mRNA and protein levels and Abeta1-42 release. Furthermore, NaHS promoted the phosphorylation of Akt and ERK but not JNK or p38 MAPK. However, the effects of NaHS on BACE-1 expression and Abeta1-42 secretion were abolished by inhibitors of phosphatidylinositol 3-kinase (PI3-K), but not of mitogen-activated protein kinase kinases (MEK). Our data indicate that H(2)S reduces BACE-1 expression in PC12 cells via activation of PI3-K/Akt signaling pathways. H(2)S releasing drugs may have therapeutic potential in AD patients.
机译：硫化氢（H（2）S）现在被确定为一种新的神经调节剂。越来越多的证据表明，H（2）S可能在阿尔茨海默氏病（AD）的进展中起重要作用。本研究的目的是研究H（2）S对PC12细胞中β-位淀粉样前体蛋白裂解酶1（BACE-1）表达和淀粉样β（Abeta）分泌的影响。通过定量聚合酶链反应分析测量BACE-1 mRNA的水平。通过蛋白质印迹评估BACE-1蛋白水平。通过ELISA分析细胞培养基Abeta1-42水平。我们发现，硫化氢钠（NaHS），H（2）S供体，减少了BACE-1 mRNA和蛋白水平以及Abeta1-42释放。此外，NaHS促进Akt和ERK的磷酸化，但不促进JNK或p38 MAPK的磷酸化。但是，NaHS对BACE-1表达和Abeta1-42分泌的影响已被磷脂酰肌醇3-激酶（PI3-K）的抑制剂所消除，而丝裂原活化的蛋白激酶激酶（MEK）的抑制剂则没有了。我们的数据表明，H（2）S通过激活PI3-K / Akt信号通路降低PC12细胞中BACE-1的表达。 H（2）S释放药物可能在AD患者中具有治疗潜力。

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