Up-regulation of peroxisome proliferator-activated receptor gamma in radiation-induced heart injury in rats

被引：0
作者：
Song Gao
Rong Wu
Yuecan Zeng
机构：
[1] Shengjing Hospital of China Medical University,Department of Clinical Oncology
来源：
Radiation and Environmental Biophysics | 2012年 / 51卷
关键词：
Pioglitazone; Myocardial Fibrosis; Irradiation Group; Masson Staining; Transform Growth Factor Type Beta1;
D O I：
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摘要：
To explore the expression level and the role of peroxisome proliferator-activated receptor gamma (PPAR-γ) in radiation-induced heart injury in a rat model, thirty-two Sprague–Dawley rats were divided into three groups (the control group, the 15-Gy irradiation group and the 18-Gy irradiation group). Experimental animals were exposed to radiation generated by a linear accelerator at the chest and killed after 3 months. Heart tissues from these animals were removed for Masson staining, PPAR-γ immunohistochemical staining, Western blot analysis and real-time polymerase chain reaction assay (RT-PCR). In addition, the protein expression of matrix metalloprotein-1 (MMP-1), tissue inhibitor of metalloproteinase-1 (TIMP-1) and transforming growth factor type beta1 (TGF-β1), all of which are associated with fibrosis, was measured. Masson staining revealed significant myocardial fibrosis, degeneration and necrosis in rats exposed to radiation. The results of immunohistochemical staining and Western blot analysis showed that PPAR-γ protein expression in hearts of the irradiation groups was significantly higher than in the control group, especially in myocardium and vascular endothelial (p < 0.05). RT-PCR results also showed a parallel increase in PPAR-γ mRNA expression in the heart of the irradiation groups compared with the control group (p < 0.05). The expression of MMP-1 protein was not significantly different in three groups (p > 0.05). The expression of TIMP-1 and TGF-β1 proteins was, however, higher in two irradiation groups than in the control group (p < 0.05). These data demonstrate that PPAR-γ expression is up-regulated on both mRNA and protein levels in heart injured by radiation. PPAR-γ may play an important role in radiation-induced heart injury.
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页码：53 / 59
页数：6
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共 169 条
[1]  
Adams MJ(2003)Radiation-associated cardiovascular disease Crit Rev Oncol Hematol 45 55-75
[2]  
Hardenbergh PH(1985)Damage to the heart from tumor irradiation in the thorax—an echocardiographic study Radiologe 25 430-436
[3]  
Constine LS(2005)Coronary heart after radiotherapy for peptic ulcer disease Int J Radiat Oncol Biol Phys 61 842-850
[4]  
Akaike A(2008)PPAR: a therapeutic target in Parkinson’s disease Neurochem 106 506-518
[5]  
Kogure T(1996)Changes in the proportion of types I and III collagen in the left ventricular wall of patients with post-irradiative pericarditis Cardiovasc Surg 4 222-226
[6]  
Oyama K(2004)Anoxia reoxygenation stimulates collagen type-I and MMP-1 expression in cardiac fibroblast s modulation by the PPAR-gamma ligand pioglitazone J Cardiovasc Pharmacol 44 682-687
[7]  
Oda M(2007)PPAR-γ agonists induce the expression of VEGF and its receptors in cultured cardiac myofibroblasts Cardiovasc Res 74 140-150
[8]  
Carr ZA(1987)Single-step method of RNA isolation by acid guanidinium thiocyanate-phenol-chloroform extraction Anal Biochem 162 156-159
[9]  
Land CE(2006)Role of PPAR in cardiovascular diseases Recent Pat Cardiovasc Drug Discov 1 193-209
[10]  
Kleinerman RA(1999)Peroxisome proliferator-activated receptor activators inhibit thrombin-induced endothelin-1 production in human vascular endothelial cells by inhibiting the activator protein-1 signaling pathway Circ Res 85 394-402
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