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Sauchinone inhibits angiotensin II‐induced proliferation and migration of vascular smooth muscle cells
Author(s) -
Wang Ying,
Li Xiaoming,
Huang Xuying,
Ma Sirui,
Xing Yue,
Geng Xiaoying,
He Xu
Publication year - 2020
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/1440-1681.13187
Subject(s) - vascular smooth muscle , angiotensin ii , vascular remodelling in the embryo , downregulation and upregulation , osteopontin , reactive oxygen species , medicine , microbiology and biotechnology , endocrinology , chemistry , biology , smooth muscle , biochemistry , blood pressure , gene
Hypertension is a common type of cardiovascular disease that remains a major cause of death in the world. Vascular remodelling is an important complication of hypertension, and vascular smooth muscle cells (VSMCs) play a major role in vascular remodelling. Sauchinone is one of the active lignins which has been found to possess vascular protective effects. However, the functional role of sauchinone in hypertension has not been investigated. The aim of this study was to evaluate the role of sauchinone in the angiotensin II (Ang II)‐induced vascular remodelling model in VSMCs. The results showed that treatment of sauchinone inhibited Ang II‐induced VSMCs proliferation and migration in VSMCs. Sauchinone treatment suppressed the reactive oxygen species (ROS) production and NADPH oxidase (NOX) activity in Ang II‐induced VSMCs. The inhibitory effects of Ang II on expressions of VSMCs phenotype markers including α‐smooth muscle actin (α‐SMA), calponin, osteopontin were mitigated by sauchinone treatment. Furthermore, sauchinone inhibited Ang II‐induced over‐activation of TGF‐β1/Smad3 signalling pathway in VSMCs. Taken together, this study identified sauchinone as a potential agent for preventing vascular remodelling in hypertension.