阿霉素性心肌病大鼠左心室肌纤维化程度与缝隙连接蛋白的变化
投稿时间:2016-09-30  修订日期:2016-10-17  点此下载全文
引用本文:单晓彤,杨晨,王伊林,柴花,赵明.阿霉素性心肌病大鼠左心室肌纤维化程度与缝隙连接蛋白的变化[J].医学研究杂志,2017,46(5):132-136
DOI: 10.11969/j.issn.1673-548X.2017.05.033
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作者单位E-mail
单晓彤 028000 通辽, 内蒙古民族大学  
杨晨 028000 通辽, 内蒙古民族大学  
王伊林 028000 通辽, 内蒙古民族大学  
柴花 028000 通辽, 内蒙古民族大学  
赵明 内蒙古民族大学附属医院 langzhe73@163.com 
基金项目:内蒙古自治区硕士研究生科研创新基金资助项目(S20161013605)
中文摘要:目的 探讨阿霉素性心肌病大鼠发生心律失常的发病机制。方法 健康wistar雄性大鼠20只,体重200g,适应周围环境1周后,随机将20只wistar雄性大鼠分为对照组(n=10)和阿霉素(ADR)组(n=10)。ADR组的大鼠在1周内进行3次腹腔注射ADR 2mg/kg;同时对照组则进行3次腹腔注射0.9%NaCl (2ml/kg),停药后让两组大鼠自由饮食4周。7周后对两组大鼠行心脏彩超检测,左心室舒张末径(LVEDd)与左心室收缩末期内径(LVESd)及左心室射血分数(LVEF),行VG染色观察各组大鼠心肌纤维化情况;扫描电镜染色观察左心室心肌细胞闰盘病理学变化;两组大鼠心肌结缔组织生长因子(CTGF)、转化生长因子β1(TGF-β1)、N型钙黏蛋白(N-cad)、桥粒芯糖蛋白(DSG2)表达应用ELISA法检测;采用Western blot法检测两组大鼠的心肌细胞Cx40 、Cx43、p-Cx43蛋白表达。结果 与对照组相比,阿霉素组大鼠明显出现心室重构,并易出现心律失常;电镜下观察ADR组大鼠心肌细胞闰盘破损严重,间隙增宽,VG染色显示ADR组大鼠病理积分明显高于对照组(P<0.05);ADR组大鼠相较于对照组大鼠心室肌中CTGF、TGF-β1的表达升高显著,N-cad、DSG2、Cx40、Cx43及p-Cx43的表达明显减低(P<0.05)。结论 ADR组大鼠可能由于心室肌细胞纤维化、闰盘结构受损、缝隙连接重构等原因导致心律失常。
中文关键词:阿霉素性心肌病  左心室纤维化  缝隙连接  闰盘
 
Mechanism of Arrhythmia in Adriamycin-Induced Cardiomyopathy Rats
Abstract:Objective Study on the pathogenesis of arrhythmia in adriamycin-induced cardiomyopathy rats. Methods Twenty healthy male wistar rats weighing 200g were randomly divided into normal control group (n=10) and doxorubicin group (n=10) after one week of adaptation. The adriamycin group received intraperitoneal injection of doxorubicin 2mg/kg intraperitoneally in one week and in the control group, 0.9% NaCl (2ml/kg) was injected intraperitoneally three times, and the rats were allowed to diet for 4 weeks after stopping. The left ventricular end-diastolic diameter, left ventricular end-diastolic thickness and left ventricular ejection fraction were measured by color Doppler ultrasonography after 7 weeks, and the myocardial fibrosis was observed by VG staining. Pathological changes of left ventricular cardiomyocytes were observed by scanning electron microscopy. The expression of connective tissue growth factor (CTGF), transforming growth factor-β1 (TGF-β1), N-cad and DSG2 in myocardium of rats were detected by ELISA. The expression of Cx40, Cx43, p-Cx43 protein was detected by Western blotting in the myocardium of the two groups. Results Compared with the control group, adriamycin group was more prone to ventricular remodeling, and more prone to arrhythmia. In the electron microscope, the damage of intercalated disc of adriamycin group was serious and the gap was widened. The pathologic score of adriamycin group was significantly higher than that of the control group by VG staining(P<0.05). The expressions of CTGF and TGF-β1 were significantly increased in the adriamycin group and the expressions of N-cad, DSG2, Cx40, Cx43 and p-Cx43 in the ventricular myocytes were significantly decreased. Conclusion Adriamycin ADR group leading to arrhythmia may be due to ventricular fibrosis, intercalated disc structure damage, gap junction remodeling and other reasons.
keywords:Adriamycin-induced cardiomyopathy  Left ventricular fibrosis  Gap junction  Intercalated disk
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