Ghrelin protects against nucleus pulposus degeneration through inhibition of NF-κB signaling pathway and activation of Akt signaling pathway.
Ghrelin protects against nucleus pulposus degeneration through inhibition of NF-κB signaling pathway and activation of Akt signaling pathway.
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Ghrelin 通过抑制 NF-kappa B 信号通路和激活 Akt 信号通路防止髓核变性
DOI：
10.18632/oncotarget.19695
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发表时间：
2017-11-03
期刊：
影响因子：
--
通讯作者：
Liu C
中科院分区：
文献类型：
--
作者：
Li W;Wu X;Qu R;Wang W;Chen X;Cheng L;Liu Y;Guo L;Zhao Y;Liu C
本研究旨在探讨ghrelin在髓核退变中的作用。在白细胞介素1β（IL-1β）刺激的人NP细胞中，Ghrelin的表达水平较低。此外，外源性ghrelin抑制IL-1β诱导的人NP细胞变性和炎症相关生物标志物，包括基质金属蛋白酶-13（一种具有血小板反应蛋白基序-5的去整合素和金属蛋白酶）、肿瘤坏死因子-α和iNOS，这可能是通过NF-κB信号的去整合化介导的。此外，ghrelin增强NP细胞的关键细胞外基质的产生，包括NP细胞中的胶原蛋白2、聚集蛋白聚糖和Sox-9。Ghrelin还促进兔IVD变性模型中的NP组织再生，这似乎与生长激素促分泌素受体有关。此外，ghrelin在抗肿瘤中的保护作用可能依赖于Akt信号通路的激活。综上所述，生长激素释放肽可能是预防和治疗椎间盘退变的分子靶点。
The objective of the present study was to examine the potential role of ghrelin in degeneration of nucleus pulposus (NP). Lower expression levels of ghrelin were found in human NP cells stimulated with interleukin-1β (IL-1β). Moreover, exogenous ghrelin suppressed IL-1β induced degeneration and inflammation associated biomarkers in human NP cells, including matrix metalloproteinase-13, a disintegrin and metalloproteinase with thrombospondin motifs-5, tumor necrosis factor-α and iNOS, which was possibly mediated by antagonization of NF-κB signaling. Moreover, ghrelin enhanced production of critical extracellular matrix of NP cells, including collagen 2, aggrecan, and Sox-9 in NP cells. Ghrelin also promoted NP tissue regeneration in a rabbit IVD degeneration model, which seems to be associated with growth hormone secretagogue receptor. Additionally, the protective role of ghrelin in anabolism potentially relies on activation of Akt signaling pathway. Taken together, ghrelin may represent a molecular target for prevention and treatment of intervertebral disc degeneration.
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