Effect of propranolol on angiopoietin and Tie2 in nude mice model with hemangioma
10.3760/cma.j.issn.1671-0290.2021.04.019
- VernacularTitle:普萘洛尔对血管瘤裸鼠模型血管生成素及Tie2的影响
- Author:
Beibei WO
1
;
Dapeng WANG
;
Jianmin YANG
Author Information
1. 解放军联勤保障部队第980医院整形外科，石家庄 050000
- Keywords:
Hemangioma;
Propranolol;
Angiopoietin;
Vascular endothelial, Growth factor;
Tie2 receptor
- From:
Chinese Journal of Medical Aesthetics and Cosmetology
2021;27(4):325-329
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the effect of propranolol on angiopoietin and its receptor in the nude mouse model of infantile hemangioma, so as to clarify the mechanism of propranolol in the treatment of hemangioma.Methods:The proliferative hemangioma tissue from the 980 Hospital of PLA was transplanted into the back of 50 female nude mice during May 2015 to Sept. 2016. After establishment of the hemangioma model, the nude mice were randomly divided into two groups, 25 in each group. The experimental group was gavaged with 0.4 ml propranolol every 2 days, and the control group was gavaged with normal saline every 2 days. The mice were killed in batches on the 7th, 14th, 21st and 28th day, the tumor morphology was observed by HE staining. The expression of VEGF, Ang1, Ang2 and Tie2 protein in hemangiomas was detected by immunohistochemistry and Western blot.Results:After 28 days, the hemangioma in propranolol group showed regression phase. The endothelial cells of hemangioma decreased, and the nuclear staining became shallow, the lumen enlarged, and fibrous connective tissue could be seen between the blood vessels. The expression of VEGF, Ang2 and Tie2 was lower than those in the control group ( P<0.05), and the expression of VEGF, Ang2 and Tie2 was decreased by 47.1%, 34.7% and 37.5%, respectively, while the expression of Ang1 was increased by 40.5% compared with the control group ( P<0.05). Conclusions:Propranolol may inhibit the growth of hemangioma in nude mice by promoting the expression of Ang1 and inhibiting the expression of VEGF, Ang2 and Tie2.
