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首页> 外文期刊>International Journal of Biomedical Science >Ghrelin Protection against Cytotoxic Effect of Ethanol on Rat Salivary Mucin Synthesis involves Cytosolic Phospholipase A2 Activation through S-Nitrosylation
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Ghrelin Protection against Cytotoxic Effect of Ethanol on Rat Salivary Mucin Synthesis involves Cytosolic Phospholipase A2 Activation through S-Nitrosylation

机译：Ghrelin对乙醇对大鼠唾液黏蛋白合成的细胞毒作用的保护作用涉及通过S-亚硝化作用激活胞质磷脂酶A 2

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摘要

Recent advances in identifying the salivary constituents of significance to the maintenance of soft oral tissue integrity have brought to focus the importance of a 28-amino acid peptide hormone, ghrelin. Here, we report on the role of ghrelin in countering the disturbances in salivary mucin synthesis caused by ethanol cytotoxicity in rat sublingual gland acinar cells. We show that the countering effect of ghrelin on mucin synthesis was associated with the increase in NO and PGE2 production, and the enhancement in cytosolic phospholipase A2 (cPLA2) activity. The ghrelin-induced up-regulation in mucin synthesis, like that of cPLA2 activity, was subject to suppression by Src inhibitor, PP2, ERK inhibitor, PD98059, as well as Akt inhibitor, SH-5 and ascorbate. Moreover, the loss in countering effect of ghrelin on the ethanol cytotoxicity and mucin synthesis was attained with cNOS inhibitor, L-NAME as well as COX-1 inhibitor, SC-560. Furthermore, while the effect of L-NAME was also reflected in the inhibition of the acinar cell capacity for NO and PGE2 generation, and cPLA2 S-nitrosylation, the COX-1 inhibitor caused the inhibition in PGE2 only. Our findings demonstrate that ghrelin protection of the acinar cells against ethanol cytotoxicity and the impairment in salivary mucin synthesis involves Src kinase activation of the Akt/cNOS pathway that leads to up-regulation in cNOS activity. We also show that cNOS-derived NO induction of the cPLA2 activation through S-nitrosylation, for the increase in PGE2 generation, is an essential element of the protective mechanism of ghrelin action.
机译：在鉴定对维持口腔软组织完整性具有重要意义的唾液成分方面的最新进展已引起人们对28种氨基酸肽激素ghrelin的重要性的关注。在这里，我们报告生长素释放肽在抵抗大鼠舌下腺腺泡细胞中乙醇细胞毒性引起的唾液粘蛋白​​合成紊乱中的作用。我们表明，ghrelin对粘蛋白合成的反作用与NO和PGE2产生的增加以及胞质磷脂酶A2（cPLA2）活性的增强有关。 ghrelin诱导的粘蛋白合成中的上调，如cPLA2活性一样，受到Src抑制剂，PP2，ERK抑制剂，PD98059以及Akt抑制剂，SH-5和抗坏血酸的抑制。而且，用cNOS抑制剂L-NAME和COX-1抑制剂SC-560获得了生长素释放肽对乙醇细胞毒性和粘蛋白合成的对抗作用的丧失。此外，虽然L-NAME的作用还体现在抑制腺泡细胞NO和PGE2生成以及cPLA2 S亚硝化的作用，但COX-1抑制剂仅引起PGE2的抑制。我们的发现表明，ghrelin保护腺泡细胞免受乙醇细胞毒性和唾液粘蛋白​​合成的损害，涉及Akt / cNOS途径的Src激酶激活，从而导致cNOS活性上调。我们还表明，cNOS衍生的NO通过c-亚硝化作用诱导cPLA2活化，以增加PGE2的生成，是生长素释放肽作用保护机制的重要组成部分。

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