我们的网站为什么显示成这样？

可能因为您的浏览器不支持样式，您可以更新您的浏览器到最新版本，以获取对此功能的支持，访问下面的网站，获取关于浏览器的信息：

|本期目录/Table of Contents|

IL-1β抑制精氨酸升压素促心脏成纤维细胞胶原凝胶的收缩

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2009年第2期
页码:
161
栏目:
基础研究
出版日期:
2009-03-30

文章信息/Info

Title:
Effects of IL-1β on collagen gel contraction induced by argipressin in cardiac fibroblasts
作者:
彭育红1; 赵连友2; 汝磊生1; 陈永清2; 范延红2; 杨学东2
1.解放军白求恩国际和平医院心内科,河北 石家庄 050082； 2.第四军医大学唐都医院心内科，陕西 西安 710038
Author(s):
PENG Yu-hong1;  ZHAO Lian-you2;  RU Lei-sheng1;  CHEN yong-qing2;  FAN yan-hong2;  YANG xue-dong2
1.Department of Cardiology, Bethune International Peace Hospital, Shijiazhuang 050082, Hebei, China; 2.Department of Cardiology, Tangdu Hospital, Fourth Military Medical University, Xi’an 710038, Shaanxi, China
关键词:
白细胞介素-1β; 精氨酸升压素; 心脏成纤维细胞; 胶原凝胶收缩
Keywords:
IL-1β;  argipressin;  cardiac fibroblasts;  collagen gel contraction
分类号:
R392.12
DOI:
-
文献标识码:
A
摘要:
目的 探讨白细胞介素-1β(IL-1β)对精氨酸升压素(AVP)诱导下心脏成纤维细胞(CF)胶原凝胶收缩的作用。方法 以胰蛋白酶消化法分离、培养SD大鼠的CF，建立成纤维细胞与胶原构成的三维培养体系，测定基础状态下不同浓度的IL-1β作用下，CF胶原凝胶收缩指数，以及IL-1β对AVP作用后CF胶原凝胶收缩指数的影响。实验共分为8个组，即不同浓度（0、50、100、200及400 kU/L）的IL-1β组、不同浓度（0、1×10-7 mol/L）的AVP干预组及100 kU/L IL-1β+1×10-7 mol/L AVP组，每组各设8个孔（n=8）。结果 在基础状态下，以50～400 kU/L IL-1β作用后，CF胶原凝胶收缩指数随着IL-1β干预浓度的增加呈下降趋势，各实验组胶原凝胶收缩指数均明显低于对照组(P<0.01)，各实验组之间两两比较的差异也非常显著(P<0.01)。1×10-7 mol/L AVP组CF胶原凝胶收缩指数明显高于0 mol/L AVP组(P<0.01)；而100 kU/L IL-1β组CF胶原凝胶收缩指数明显低于0 kU/L IL-1组(P<0.01)。IL-1β与AVP共同作用后，CF胶原凝胶收缩指数介于AVP组和IL-1β组之间，并且与二者之间的差异均有非常显著的意义(P<0.01)。结论 IL-1β可抑制基础状态下CF胶原凝胶收缩，并对AVP促CF胶原凝胶收缩具有明显的拮抗作用。
Abstract:
AIM To explore the effects of interleukin(IL)-1β on collagen gel contraction induced by argipressin (AVP) in cardiac fibroblasts (CF). METHODS Using trypsin separate and culture cardiac fibroblasts (CF) of SD neonatal rats, we set up a three-dimensional culture system of CF and collagen gel. RESULTS With the pretreatment with IL-1β (50~400 kU/L) in CF, the collagen gel contraction index decreased with the increasing concentration of IL-1β, and the index in each test group was significantly lower than that in control (P<0.01). The collagen gel contraction index of pretreatment with AVP was significantly higher than that in control (P<0.01) whereas the index of pretreatment with IL-1β was significantly lower than that in control (P<0.01). Following simultaneous pretreatment with AVP and IL-1β, the index was between those of the two groups, with significant difference between AVP or IL-1β (P<0.01). CONCLUSION IL-1β inhibits collagen gel contraction in basic condition and antagonizes the effects of AVP on collagen gel contraction.

参考文献/References

[1］ Dinarello CA. Interleukin-1 and interleukin-1 antagonism［J］. Blood, 1991, 77(8):1627-1652.

［2］ 徐海丽,赵连友. IL-I β对精氨酸加压素诱导心脏成纤维细胞胶原合成的抑制作用［J］. 细胞与分子免疫学杂志， 2000, 16(3):234-236.

［3］ 赵连友,徐海丽,杨学东,等. IL-I β对精氨酸加压素诱导心脏成纤维细胞增殖的抑制作用［J］ . 第四军医大学学报, 2001, 22(21):2003-2006.

［4］ Gullberg D, Tingstrom A, Thuresson A, et al. β1 Integrin-mediated collagen gel contraction is stimulated by PDGF［J］. Exp Cell Res, 1990, 186(2):264-272.

［5］ Handing P, Carretero OA, LaPointe MC. Effects of interleukin-1β and nitric oxide on cardiac myocytes［J］. Hypertension, 1995, 25(3):421-430.

［6］ Nunohiro T, Ashizawa N, Graf K, et al. Angiotensin II promotes integrin-mediated collagen gel contraction by adult rat cardiac fibroblasts［J］. Jpn Heart J, 1999, 40(4):461-469.

［7］ 彭育红,赵连友,陈永清,等. 反义β1整合素寡核苷酸对精氨酸加压素促胶原凝胶收缩的抑制作用［J］. 心脏杂志, 2001, 13(2):112-114.［8］ Kacimi R, Long CS, Karliner JS. Chronic hypoxia modulates the interleukin-1β-stimulated inducible nitric oxide synthase pathway in cardiac myocytes［J］. Circulation, 1997, 96(6):1937-1943.

［9］ Jiang B, Brecher P. N-Acetyl-L-Cysteine potentiates interleukin-1β induction of nitric oxide synthase: role of p44/42mitogen-activated protein kinase［J］. Hypertension, 2000, 35(4):914-918.

［10］Jiang B, Haverty M, Brecher P, et al. N-acetyl-L-cysteine enhances interleukin-1β-induced nitric oxide synthase expression［J］. Hypertension, 1999, 34(4 Pt 1): 574-579.

［11］He Q, LaPointe MC. Interleukin-1β regulates the human brain natriuretic peptide promoter via Ca2+-development protein kinase pathways［J］. Hypertension, 2000, 35(1 Pt 2): 292-296.

［12］Karna E, Miltyk W, Paka JA, et al. Hyaluronic acid counteracts interleukin-1-induced inhibition of collagen biosynthesis in cultured human chondrocytes［J］. Pharmacol Res, 2006,54(4):275-281.

［13］Karna E, Miltyk W, Surazyński A, et al. Protective effect of hyaluronic acid on interleukin-1-induced deregulation of beta1-integrin and insulin-like growth factor-I receptor signaling and collagen biosynthesis in cultured human chondrocytes［J］. Mol Cell Biochem, 2008, 308(1-2):57-64.

备注/Memo

备注/Memo:
收稿日期：2008-8-26.通讯作者:赵连友,主任医师,主要从事冠心病及高血压病基础与临床的研究Email:zhaoly.fmmu@yahoo.com.cn 作者简介:彭育红,主治医师，硕士Email:pyh1a@Yahoo.com.cn
更新日期/Last Update: 2009-04-16