Li Shuangdi, Dong Jingrong, Ta Guang, Liu Yinghui, Cui Junfeng, Li Xiaohui, Song Jing, Liu Aidong, Cheng Guangyu
Center of Heart Disease, Affiliated Hospital of Changchun University of Traditional Chinese Medicine, Changchun, China.
Department of Endoscopy, Affiliated Hospital of Changchun University of Traditional Chinese Medicine, Changchun, China.
Evid Based Complement Alternat Med. 2020 Feb 5;2020:5041629. doi: 10.1155/2020/5041629. eCollection 2020.
To investigate the effect of Xuan Bi Tong Yu Fang (XBTYF) on angiogenesis via the vascular endothelial growth factor- (VEGF-) Notch1/delta-like 4 (Dll4) pathway. . Sixty Sprague-Dawley rats were randomly divided into six groups: control, sham-operated, myocardial ischemia model, and XBTYF treatment at 3.2, 1.6, and 0.8 g/kg. Electrocardiography was performed to evaluate the successful establishment of the model. Hematoxylin-eosin staining and transmission electron microscopy were carried out to observe the morphology and mitochondrial structure in myocardial cells, respectively. TUNEL staining was performed to assess the degree of cell apoptosis. The expression of VEGF-A, Notch1, Dll4, Bcl2, Bax, caspase 3, caspase 9, and cytochrome-c (Cyt-c) was observed by western blot.
XBTYF inhibited changes to the morphology and mitochondrial structure in cardiomyocyte and reduced cell apoptosis. Compared with the model group, XBTYF at all doses (3.2, 1.6, and 0.8 g/kg) reduced the expression of Notch1, Dll4, Bax, caspase 3, caspase 9, and Cyt-c, whereas expression of VEGF-A and Bcl2 was increased.
XBTYF attenuated mitochondrial damage and cell apoptosis while promoting the angiogenesis of cardiomyocyte. The associated mechanism may be related to the VEGF-Notch1/Dll4 pathway.
通过血管内皮生长因子（VEGF）-Notch1/Delta样蛋白4（Dll4）通路研究宣痹通瘀方（XBTYF）对血管生成的影响。将60只Sprague-Dawley大鼠随机分为六组：对照组、假手术组、心肌缺血模型组以及XBTYF 3.2、1.6和0.8 g/kg治疗组。通过心电图评估模型的成功建立。分别进行苏木精-伊红染色和透射电子显微镜检查以观察心肌细胞的形态和线粒体结构。采用TUNEL染色评估细胞凋亡程度。通过蛋白质免疫印迹法观察VEGF-A、Notch1、Dll4、Bcl2、Bax、半胱天冬酶3、半胱天冬酶9和细胞色素c（Cyt-c）的表达。
XBTYF抑制心肌细胞形态和线粒体结构的改变并减少细胞凋亡。与模型组相比，所有剂量（3.2、1.6和0.8 g/kg）的XBTYF均降低了Notch1、Dll4、Bax、半胱天冬酶3、半胱天冬酶9和Cyt-c的表达，而VEGF-A和Bcl2的表达增加。
XBTYF减轻线粒体损伤和细胞凋亡，同时促进心肌细胞血管生成。相关机制可能与VEGF-Notch1/Dll4通路有关。
