Protective Effect of Angiotensin (1-7) on Silicotic Fibrosis in Rats.

Bo Nan Zhang; Hong XU; Xue Min Gao; Gui Zhen Zhang; Xin Zhang; Fang Yang

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Protective Effect of Angiotensin (1-7) on Silicotic Fibrosis in Rats.

Author: Bo Nan ZHANG ^{1
,

2
,

3} ; Hong XU ⁴ ; Xue Min GAO ⁵ ; Gui Zhen ZHANG ^{3
,

6} ; Xin ZHANG ⁴ ; Fang YANG ⁴
Author Information

1. School of Public Health, North China University of Science and Technology, Tangshan 063210, Hebei, China
2. Hebei Key Laboratory for Organ Fibrosis, Medical Research Center, North China University of Science and Technology, Tangshan 063210, Hebei, China
3. Hebei Key Laboratory for Chronic Diseases, Tangshan Key Laboratory for Clinical and Basic Research on Chronic Diseases, School of Basic Medical Sciences, North China University of Science and Technology, Tangshan 063210, Hebei, China.
4. Hebei Key Laboratory for Organ Fibrosis, Medical Research Center, North China University of Science and Technology, Tangshan 063210, Hebei, China.
5. Basic Medical College, Hebei Medical University, Shijiazhuang 050017, Hebei, China.
6. Hebei Key Laboratory for Organ Fibrosis, Medical Research Center, North China University of Science and Technology, Tangshan 063210, Hebei, China
Publication Type:Journal Article
Keywords: A779; Ang (1-7); Ang II; Myofibroblasts; Silicosis
MeSH: Actins; metabolism; Angiotensin I; blood; pharmacology; therapeutic use; Angiotensin II; blood; Animals; Animals, Newborn; Cell Differentiation; drug effects; Cells, Cultured; Collagen Type I; metabolism; Disease Models, Animal; Lung; metabolism; pathology; Myofibroblasts; drug effects; Peptide Fragments; blood; pharmacology; therapeutic use; Peptidyl-Dipeptidase A; metabolism; Rats, Wistar; Silicosis; metabolism; pathology; prevention & control
From: Biomedical and Environmental Sciences 2019;32(6):419-426
CountryChina
Language:English
Abstract: OBJECTIVE:Silicosis, caused by inhalation of silica dust, is the most serious occupational disease in China and the aim of present study was to explore the protective effect of Ang (1-7) on silicotic fibrosis and myofibroblast differentiation induced by Ang II.
METHODS:HOPE-MED 8050 exposure control apparatus was used to establish the rat silicosis model. Pathological changes and collagen deposition of the lung tissue were examined by H.E. and VG staining, respectively. The localizations of ACE2 and α-smooth muscle actin (α-SMA) in the lung were detected by immunohistochemistry. Expression levels of collagen type I, α-SMA, ACE2, and Mas in the lung tissue and fibroblasts were examined by western blot. Levels of ACE2, Ang (1-7), and Ang II in serum were determined by ELISA. Co-localization of ACE2 and α-SMA in fibroblasts was detected by immunofluorescence.
RESULTS:Ang (1-7) induced pathological changes and enhanced collagen deposition in vivo. Ang (1-7) decreased the expressions of collagen type I and α-SMA and increased the expressions of ACE2 and Mas in the silicotic rat lung tissue and fibroblasts stimulated by Ang II. Ang (1-7) increased the levels of ACE2 and Ang (1-7) and decreased the level of Ang II in silicotic rat serum. A779 enhanced the protective effect of Ang (1-7) in fibroblasts stimulated by Ang II.
CONCLUSION:Ang (1-7) exerted protective effect on silicotic fibrosis and myofibroblast differentiation induced by Ang II by regulating ACE2-Ang (1-7)-Mas axis.