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本文引用的文献

1
Aging in rat causes hepatic hyperresposiveness to interleukin-1beta which is mediated by neutral sphingomyelinase-2.衰老使大鼠肝脏对白介素-1β产生高反应性，这是由中性鞘磷脂酶-2介导的。
Hepatology. 2007 Oct;46(4):1166-76. doi: 10.1002/hep.21777.
2
Clinical implications of the reduced activity of the GH-IGF-I axis in older men.老年男性生长激素-胰岛素样生长因子-I轴活性降低的临床意义。
J Endocrinol Invest. 2005;28(11 Suppl Proceedings):96-100.
3
Control of aging and longevity by IGF-I signaling.胰岛素样生长因子-I信号通路对衰老和寿命的调控。
Exp Gerontol. 2005 Nov;40(11):867-72. doi: 10.1016/j.exger.2005.08.001. Epub 2005 Sep 8.
4
Roles of insulin-like growth factor (IGF) binding proteins in regulating IGF actions.胰岛素样生长因子（IGF）结合蛋白在调节IGF作用中的角色。
Gen Comp Endocrinol. 2005 May 15;142(1-2):44-52. doi: 10.1016/j.ygcen.2004.12.022. Epub 2005 Feb 5.
5
Expression of neutral sphingomyelinase-2 (NSMase-2) in primary rat hepatocytes modulates IL-beta-induced JNK activation.原代大鼠肝细胞中中性鞘磷脂酶-2（NSMase-2）的表达调节白细胞介素-β诱导的JNK激活。
FASEB J. 2004 Jun;18(9):968-70. doi: 10.1096/fj.03-0875fje. Epub 2004 Apr 1.
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Insights from insulin-like growth factor binding protein transgenic mice.
Endocrinology. 2002 Oct;143(10):3711-4. doi: 10.1210/en.2002-220116.
7
Analyzing JNK and p38 mitogen-activated protein kinase activity.分析JNK和p38丝裂原活化蛋白激酶活性。
Methods Enzymol. 2001;332:319-36. doi: 10.1016/s0076-6879(01)32212-7.
8
(R)-alpha-lipoic acid reverses the age-associated increase in susceptibility of hepatocytes to tert-butylhydroperoxide both in vitro and in vivo.（R）-α-硫辛酸在体外和体内均可逆转与年龄相关的肝细胞对叔丁基过氧化氢敏感性增加的现象。
Antioxid Redox Signal. 2000 Fall;2(3):473-83. doi: 10.1089/15230860050192251.
9
Activation of sphingolipid turnover and chronic generation of ceramide and sphingosine in liver during aging.衰老过程中肝脏内鞘脂代谢的激活以及神经酰胺和鞘氨醇的慢性生成。
Mech Ageing Dev. 2000 Dec 1;120(1-3):111-25. doi: 10.1016/s0047-6374(00)00191-3.
10
Stimulation of insulin-like growth factor binding protein-1 synthesis by interleukin-1beta: requirement of the mitogen-activated protein kinase pathway.
Endocrinology. 2000 Sep;141(9):3156-64. doi: 10.1210/endo.141.9.7641.

衰老过程中胰岛素样生长因子结合蛋白-1表达的调控。

Regulation of insulin-like growth factor binding protein-1 expression during aging.

作者信息

Rutkute Kristina, Nikolova-Karakashian Mariana N

机构信息

Department of Physiology, University of Kentucky College of Medicine, A.B. Chandler Medical Center, 800 Rose St., Lexington, KY 40536, USA.

出版信息

Biochem Biophys Res Commun. 2007 Sep 21;361(2):263-9. doi: 10.1016/j.bbrc.2007.06.079. Epub 2007 Jun 21.

DOI:10.1016/j.bbrc.2007.06.079
PMID:17645865
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2017095/
Abstract

Insulin-like growth factor (IGF) binding protein-1 (IGFBP-1) is primarily produced in the liver during inflammation and regulates biological activities of IGF-I. Here we demonstrate that interleukin-1beta (IL-1beta) stimulates IGFBP-1 mRNA production in a dose-dependent manner in hepatocytes from Fisher 344 rats. Employment of c-Jun N-terminal kinase (JNK) inhibitor SP600125 resulted in 3-fold reduction of IGFBP-1 mRNA and protein levels, indicating that IL-1beta-induced IGFBP-1 production is mediated through JNK activation. We further show that hepatocytes from aged rats (20-22 mo), as compared to young (3-4 mo), exhibit up to 2-fold higher levels of IGFBP-1 in response to IL-1beta. IL-1beta-induced phosphorylation of JNK was also significantly higher in aged hepatocytes, and SP600125 treatment eliminated age-related differences in IGFBP-1 mRNA production. Moreover, glutathione depletion in hepatocytes from young rats potently activated JNK, as well as increased IL-1beta-induced IGFBP-1 mRNA levels, suggesting that age-related oxidative stress underlies the upregulated JNK activation and IGFBP-1 expression.

摘要

胰岛素样生长因子（IGF）结合蛋白-1（IGFBP-1）主要在炎症期间由肝脏产生，并调节IGF-I的生物学活性。在此我们证明，白细胞介素-1β（IL-1β）以剂量依赖的方式刺激来自Fisher 344大鼠的肝细胞中IGFBP-1 mRNA的产生。使用c-Jun N端激酶（JNK）抑制剂SP600125导致IGFBP-1 mRNA和蛋白水平降低3倍，表明IL-1β诱导的IGFBP-1产生是通过JNK激活介导的。我们进一步表明，与年轻大鼠（3-4个月）相比，老年大鼠（20-22个月）的肝细胞对IL-1β的反应中IGFBP-1水平高出2倍。老年肝细胞中IL-1β诱导的JNK磷酸化也显著更高，并且SP600125处理消除了IGFBP-1 mRNA产生中的年龄相关差异。此外，年轻大鼠肝细胞中的谷胱甘肽耗竭有力地激活了JNK，并增加了IL-1β诱导的IGFBP-1 mRNA水平，表明年龄相关的氧化应激是JNK激活上调和IGFBP-1表达增加的基础。