C57BL/6小鼠放射性心肺功能不全动物模型建立

Establishment of C57BL/6 mouse models with radiation-induced cardiopulmonary dysfunction

目的建立C57BL/6小鼠放射性心肺功能不全动物模型。方法24只雄性C57BL/6小鼠随机分为对照组、照射组。照射组接受胸部局部单次20 Gy电子线照射,照后饲养6个月。超声心动检查心功能,血气分析检测血氧分压(PaO2),Tunel染色法检测细胞凋亡,Masson染色法检测心肺纤维化。结果照射组LVEF(68.60±10.92)%与对照组(81.75±8.79)%降低(P<0.01);照射组心脏凋亡指数(23.90±6.60)%比对照组(3.25±3.38)%增高(P<0.01);照射组心脏CVF(15.42±5.72)%比对照组(1.45±0.64)%增高(P<0.01)。照射组PaO2(86.10±7.60)mmHg比对照组PaO2(107.16±9.01)mmHg下降(P<0.01);照射组肺脏凋亡指数(27.90±8.94)%比对照组(2.50±3.55)%增高(P<0.01);照射组肺脏CVF(17.76±5.77)%比对照组(2.50±3.55)%增高(P<0.01)。结论辐射使心肺凋亡纤维化重塑,进而导致心肺功能的下降,成功构建C57BL/6小鼠放射性心肺功能不全动物模型。

Objective To establish the C57BL/6 mouse models of radiation-induced cardiopulmonary dysfunction.Methods Twenty-four male C57BL/6 mice were randomly divided into the control and irradiation groups.Mice in the irradiation group were irradiated with 20 Gy electron beam and bred for 6 months after irradiation.Cardiac function was assessed using ultrasonography.The partial pressure of oxygen was detected by blood gas analysis.Cell apoptosis was observed by Tunel assay.Myocardial and pulmonary fibrosis was assessed by Masson staining.Results The LVEF in the irradiation group was(68.60±10.92)%,significantly less compared with(81.75±8.79)%in the control group(P<0.01).The apoptotic index of heart in the irraiation group was(23.90±6.60)%,considerably higher than(3.25±3.38)%in the control group(P<0.01).The CVF of heart in the irradiation group was(15.42±5.72)%,significantly higher than(1.45±0.64)%in the control group(P<0.01).The PaO2 level in the irradiation group was(86.10±7.60)mmHg,significantly lower compared with(107.16±9.01)mmHg in the control group(P<0.01).The apoptotic index of lung in the irradiation group was(27.90±8.94)%,significantly higher than(2.50±3.55)%in the control group(P<0.01).The CVF of lung in the irradiation group was(17.76±5.77)%,remarkably higher than(2.50±3.55)%in the control group(P<0.01).Conclusion Radiation can induce cardiopulmonary apotosis and fibrosis remodeling,which leads to cardiopulmonary dysfunction,suggesting the successful establishment of C57BL/6 mouse model of radiation-induced cardiopulmonary dysfunction.