| 旷华香,徐世林,欧阳伟炜,等.重组人血管内皮抑制素对大鼠放射性心肌纤维化的影响[J].中华放射医学与防护杂志,2020,40(5):343-348.Kuang Huaxiang,Xu Shilin,Ouyang Weiwei,et al.Recombinant human endostatin reduces radiation-induced myocardial fibrosis in rats[J].Chin J Radiol Med Prot,2020,40(5):343-348 |
| 重组人血管内皮抑制素对大鼠放射性心肌纤维化的影响 |
| Recombinant human endostatin reduces radiation-induced myocardial fibrosis in rats |
| 投稿时间：2019-09-13 |
| DOI：10.3760/cma.j.issn.0254-5098.2020.05.003 |
| 中文关键词: 重组人血管内皮抑制素 放射 心脏 纤维化 |
| 英文关键词:Recombinant human endostatin Radiation Heart Fibrosis |
| 基金项目:国家自然科学基金（81660507）；贵州省科技支撑计划项目（[2018]2755） |
| 作者 | 单位 | E-mail | | 旷华香 | 苏胜发 贵州医科大学附属医院肿瘤科 贵州医科大学肿瘤学教研室 贵州省肿瘤医院肿瘤科, 贵阳 550004 | | | 徐世林 | 苏胜发 贵州医科大学附属医院肿瘤科 贵州医科大学肿瘤学教研室 贵州省肿瘤医院肿瘤科, 贵阳 550004 | | | 欧阳伟炜 | 苏胜发 贵州医科大学附属医院肿瘤科 贵州医科大学肿瘤学教研室 贵州省肿瘤医院肿瘤科, 贵阳 550004 | | | 赵朝芬 | 苏胜发 贵州医科大学附属医院肿瘤科 贵州医科大学肿瘤学教研室 贵州省肿瘤医院肿瘤科, 贵阳 550004 | | | 李晓阳 | 苏胜发 贵州医科大学附属医院肿瘤科 贵州医科大学肿瘤学教研室 贵州省肿瘤医院肿瘤科, 贵阳 550004 | | | 陈霞霞 | 苏胜发 贵州医科大学附属医院肿瘤科 贵州医科大学肿瘤学教研室 贵州省肿瘤医院肿瘤科, 贵阳 550004 | | | 杨文刚 | 苏胜发 贵州医科大学附属医院肿瘤科 贵州医科大学肿瘤学教研室 贵州省肿瘤医院肿瘤科, 贵阳 550004 | | | 马筑 | 苏胜发 贵州医科大学附属医院肿瘤科 贵州医科大学肿瘤学教研室 贵州省肿瘤医院肿瘤科, 贵阳 550004 | | | 卢冰 | 苏胜发 贵州医科大学附属医院肿瘤科 贵州医科大学肿瘤学教研室 贵州省肿瘤医院肿瘤科, 贵阳 550004 | | | 苏胜发 | 苏胜发 贵州医科大学附属医院肿瘤科 贵州医科大学肿瘤学教研室 贵州省肿瘤医院肿瘤科, 贵阳 550004 | sushengfa2005@163.com |
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| 中文摘要: |
| 目的 建立放射性心脏纤维化大鼠模型，观察重组人血管内皮抑制素（恩度）对心肌纤维化的影响，初探转化生长因子-β1（TGF-β1）、结缔组织生长因子（CTGF）与心肌纤维化的相关性。方法 将40只SD大鼠按随机数表法分为4组，每组10只，A组为健康对照组；B组为恩度干预组，恩度（6 mg/kg）腹腔连续注射14 d；C组为单纯照射组，心脏照射25 Gy/5次，连续5 d；D组为照射+恩度干预组，恩度给药方法同B组、心脏照射方法同C组。照射后第1、3个月各麻醉处死5只大鼠。Masson染色评估心肌纤维化情况，Western blot检测心肌TGF-β1、CTGF及胶原蛋白Ⅰ（COL-Ⅰ）型表达。结果 照射后1和3个月，B组未见明显的心肌纤维化表现，C组和D组可见胶原纤维分布于心肌细胞间质。照射后1个月，半定量分析结果显示A组的心肌胶原容积分数（CVF）为（5.20±0.75）%，C组（10.12±2.17）%和D组（10.32±1.36）均高于A组（t=4.74、4.93，P<0.01），C组和D组的CVF差异无统计学意义（P>0.05）；照射后3个月C组的CVF（13.17±2.67）%仍比A组（5.23±1.32）%高（t=4.49，P<0.01），C组的CVF低于D组（16.92±3.58）%（t=3.19，P<0.05）。照射后1个月，A组TGF-β1的表达量为0.441±0.063，C组0.817±0.079高于A组（t=5.81，P<0.01）；照射后3个月，A组TGF-β1的表达量为0.501±0.110，C组0.832±0.150高于A组（t=4.19，P<0.01），D组1.403±0.133高于C组（t=7.24，P<0.01）。照射后1、3个月，各组间CTGF及COL-I的变化趋势与TGF-β1的变化趋势相似。结论 射线可引起心肌纤维化的形成，重组人血管内皮抑制素可能会加重晚期放射纤维化的形成。 |
| 英文摘要: |
| Objective To assess the effects of recombinant human endostatin (rh-ES) on radiation-induced myocardial fibrosis. Methods Totally 40 SD rats were randomly divided into 4 groups, including A group as normal control, B group receiving rh-ES with a dosage of 6 mg·kg-1·d-1, in traperitoneal injection, for 14 consecutive days, C group with local heart irradiation delivered to the precordial region of rats in five fractions with a dose of 25 Gy, D group receiving rh-ES as the same as B group and local heart irradiation as C group. At 1 and 3 months after irradiation, five rats were killed under anesthesia. Mason staining was used to observe myocardial injury and fibrosis. Western blotting was used to detect the expression of TGF-β1, CTGF and COL-I in myocardium. Results Masson staining showed that no obvious myocardial fibrosis was found in group B at 1 month and 3 months after irradiation, while collagen fibers were distributed in myocardium in groups C and D. One month after irradiation, the result of semi-quantitative analysis showed that the CVF in group A was (5.20 ±0.75)%, which was significantly lower than that in group C (10.12 ±2.17)% (t=4.74、4.93,P<0.01) and the CVF in group D (10.32 ±1.36),and the CVF of group C was similar to that of group D (P<0.01). Three months after irradiation, CVF in group C (13.17±2.67)% was still higher than that in group A (5.23 ±1.32)% (t=4.49, P<0.01), but lower than that in group D (16.92 ±3.58)% (t=3.19,P<0.05). One month after irradiation, the expression of TGF-β1 in group A was 0.441 ±0.063, lower than that in group C (0.817 ±0.079, t=5.81, P<0.01). Three months after irradiation, the expression of TGF-β1 in group A was 0.501 ±0.110, lower than that in group C (0.832 ±0.150, t=4.19,P<0.01), and the expression of TGF-β1 in group D was 1.403 ±0.133, which was significantly higher than that in group C (t=7.24, P<0.01). Conclusions Radiation can cause the formation of myocardial fibrosis, and recombinant human endostatin may aggravate the formation of late radiation fibrosis. |
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