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|本期目录/Table of Contents|

肿瘤坏死因子α对新生大鼠心肌成纤维细胞增殖的影响及其机制

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2009年第5期
页码:
621-624
栏目:
基础研究
出版日期:
2009-07-14

文章信息/Info

Title:
Effect of TNF-α on proliferation of rat cardiac fibroblasts and its underlying mechanism
作者:
张杰; 杨国栋; 卢兹凡
第四军医大学生物化学与分子生物学教研室，陕西 西安 710032
Author(s):
ZHANG Jie;  YANG Guo-dong;  LU Zi-fan
Department of Biochemistry and Molecular Biology, Fourth Military Medical University, Xian 710032, Shaanxi, China
关键词:
肿瘤坏死因子-α; 心肌成纤维细胞; 周期蛋白D1; 增殖
Keywords:
tumor necrosis factor-α;  cardiac fibroblast;  cyclinD1;  proliferation
分类号:
R392.12
DOI:
-
文献标识码:
A
摘要:
目的: 探讨肿瘤坏死因子α（TNF-α）刺激对新生大鼠心肌成纤维细胞（CFs）增殖的影响及其机制。方法: 采用消化法培养新生SD大鼠的CFs。实验分为4组，即5、10和20 μg/L TNF-α处理组及空白对照组。将CFs培养36 h后，用四氮唑蓝(MTT)比色法测定细胞的增殖；分别用半定量RT-PCR和Western blot技术检测在5 μg/L和10 μg/L TNF-α刺激下细胞周期蛋白D1（CyclinD1 mRNA及其蛋白）表达的变化。结果: 随着TNF-α浓度的增高，MTT比色法检测的A490值呈明显递增趋势，其中5、10及 20 μg/L组的A490值，分别为0.417±0.011、0.622±0.015和0.602±0.013，与对照组（0.235±0.013）相比，有显著差异（P<0.05）。RT-PCR和免疫印迹检测表明，以5 μg/L和10 μg/L TNF-α刺激36 h后，CyclinD1 mRNA(0.706±0.113,1.698±0.135)和其蛋白(1.270±0.168,2.749±0.170)的水平均明显高于对照组CyclinD1mRNA(0.192±0.039)和蛋白（0.658±0.101）的表达水平（均P<0.01）。结论: TNF-α可通过上调CyclinD1的表达促进心肌成纤维细胞增殖，这可能为应用TNF-α信号通路抑制剂进行抗心肌纤维化治疗提供实验依据。
Abstract:
AIM: To investigate the effects of tumor necrosis factor α (TNF-α) on the proliferation of cardiac fibroblast (CF) and the underlying mechanism. METHODS: CFs of neonatal Sprague Dawley rats were isolated by enzymatic dissociation. CF proliferation was measured by thiazolyl blue (MTT) assay and expression of cyclinD1 was detected by RT-PCR and Western blotting. RESULTS: MTT colorimetry showed that the A490 values were 0.417±0.011, 0.622±0.015 and 0.602±0.013, respectively in the 5 μg/L, 10 μg/L and 20 μg/L TNF-α groups, all significantly higher than that in the control group (0.235±0.013, all P<0.05). After stimulation of 5 μg/L and 10 μg/L TNF-α for 36 h, cyclinD1 was upregulated both in mRNA (0.706±0.113, 1.698 ± 0.135) and protein (1.270±0.168, 2.749±0.170) levels compared with those in control group (0.192±0.039 and 0.658±0.101) (all P<0.01). CONCLUSION: Tumor necrosis factor-α promotes CF proliferation through upregulation of cyclinD1. Our findings may provide evidence of using TNF-α signal pathway inhibitor for anti-fibrosis.

参考文献/References

［1］ Nishimura T, Faul JL, Berry GJ, et al. Simvastatin attenuates smooth muscle neointimal proliferation and pulmonary hypertension in rats［J］. Am J Respir Crit Care Med, 2002,166(10):1403-1408.

［2］ Girgis RE, Mozammel S, Champion HC, et al. Regression of chronic hypoxic pulmonary hypertension by simvastatin［J］. Am J Physiol Lung Cell Mol Physiol, 2007, 292(5):L1105-L1110.

［3］ Jiang BH, Tawara S, Abe K, et al. Acute vasodilatou effect of fasudil,a Rho-kinase inhibitor, in monocrotaline-induced pulmonary hypertension in rats［J］. J Cardiovasc Pharmacol, 2007, 49(2):85-89.

［4］ Dannenberg AJ, Altorki NK, Boyle JO, et al. Cyclooxygenase 2: a pharmacological target for the prevention of cancer［J］. Lancet Oncol, 2001, 2(9):544-551.

备注/Memo

备注/Memo:
收稿日期：2009-4-27.基金项目：国家自然科学基金项目资助(30271457) 通讯作者：卢兹凡，教授，主要从事疾病相关信号传导网络研究Email:luzfliuq@fmmu.edu.cn 作者简介：张杰，硕士Email:jacky29@fmmu.edu.cn
更新日期/Last Update: 2009-07-22