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Zhonghua Gan Zang Bing Za Zhi. 2013 Dec;21(12):907-13. doi: 10.3760/cma.j.issn.1007-3418.2013.12.007.

[Inhibitory effect of angiotensin (1-7) on hepatic sinusoid angiogenesis in bile duct ligation-induced hepatic fibrosis of rats].

[Article in Chinese]

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Emergency Department, Nanfang Hospital of Nanfang Medical University, Guangzhou 510515, China.



To explore the inhibitory effect of angiotensin (1-7) on hepatic sinusoid angiogenesis using a rat model of hepatic fibrosis.


Eighteen male Wistar rats were randomly divided into three equal groups for sham operation (untreated/uninduced control group), bile duct ligation (BDL) (untreated model group), or BDL with angiotensin (1-7) treatment (treated model group). Histological analysis was used to assess the liver fibrosis score, by hematoxylin-eosin staining, and the level of fibrosis, by Masson's trichrome staining. Immunohistochemistry, western blotting, and immunofluorescence were used to assess the expression of the angiogenesis markers vWF, VEGFA, and CD31.


Compared with the untreated/uninduced control group, the untreated BDL model group showed remarkably higher fibrosis score, area of the type I collagen expression, and expression levels of vWF, VEGFA, and CD31. However, the angiotensin (1-7)-treatment protected against the BLD-related changes, as evidenced by decreased robustness and down-regulation of the corresponding indicators. Moreover, the expression level of VEGFA was highly correlated to the expression level of vWF (r = 0.956, P = 0.000).


BDL-induced hepatic fibrosis is accompanied by significant increases in angiogenesis-related factors, but angiotensin (1-7) treatment may inhibit hepatic sinusoid angiogenesis during the liver fibrosis process.

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