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DOI 10.11817/j.issn.1672-7347.2017.03.001

Медицинская библиотека · Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2017

[Effect of nucleolin on cardiac cell apoptosis in Type 2 diabetic cardiomyopathy mice].

Liu Meidong, Sun Li, Jiang Bimei, Tan Sipin, Liu Ke, Xiao Xianzhong

СтатьяПеревод пока не подготовлен

Аннотация

To investigate the effect of nucleolin on cardiac cell apoptosis in Type 2 diabetic cardiomyopathy mice.

Methods

Mice were fed with high-fat and high-sugar food for 20 weeks (mice were injected intraperitoneally with 60 mg/kg streptozotocin in the 5th and 6th weeks) to establish a mouse model of Type 2 diabetes. The mice were divided into 4 groups: a wild type (WT) control group, a nucleolin transgenic (TG) control group, a WT diabetic group, a TG diabetic group. Diabetes-related indicators were detected at the end of the 8th week. At the end of the 20th week, HE staining was used to observe myocardial morphological changes; TUNEL staining and caspase-3 activity were used to detect the extent of apoptosis of cardiac myocytes.

Results

The level of fasting blood glucose was significantly increased in the diabetic group than that in the control group. In WT diabetic group, myocardial disarrangement, fragmentation and dissolution were observed (determined by HE staining); cellular apoptosis (determined by TUNEL staining and caspase-3 activity) also increased markedly in the WT diabetic group. Compared with the wild mice in the diabetic group, myocardial morphological changes and cardiac myocytes apoptosis were alleviated significantly.

Conclusion

Nucleolin overexpression affectes the occurrence and development of diabetic cardiomyopathy through inhibition of cardiac myocyte apoptosis.

Для цитирования: Liu Meidong, Sun Li, Jiang Bimei, Tan Sipin, Liu Ke, Xiao Xianzhong. [Effect of nucleolin on cardiac cell apoptosis in Type 2 diabetic cardiomyopathy mice].. Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences. 2017. DOI: 10.11817/j.issn.1672-7347.2017.03.001.

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