Uncaria Rhynchophylla attenuates angiotensin II-induced myocardial fibrosis via suppression of the RhoA/ROCK1 pathway

被引:9
|
作者
Xie, Lingling [1 ,2 ,3 ]
Wang, Tianyi [1 ,2 ,3 ]
Lin, Shan [1 ,2 ,3 ]
Lu, Zhuqing [1 ,2 ,3 ]
Wang, Yilian [1 ,2 ,3 ]
Shen, Zhiqing [4 ]
Cheng, Ying [1 ,2 ,3 ]
Shen, Aling [1 ,2 ,3 ]
Peng, Jun [1 ,2 ,3 ]
Chu, Jianfeng [1 ,2 ,3 ]
机构
[1] Fujian Univ Tradit Chinese Med, Acad Integrat Med, 1 Qiuyang Rd, Fuzhou 350122, Fujian, Peoples R China
[2] Fujian Univ Tradit Chinese Med, Fujian Key Lab Integrat Med Geriatr, Fuzhou 350122, Fujian, Peoples R China
[3] Fujian Univ Tradit Chinese Med, Chen Keji Acad Thought Inheritance Studio, Fuzhou 350122, Fujian, Peoples R China
[4] Fujian Tradit Med Univ, Peoples Hosp, 602,817 Middle Rd, Fuzhou 350004, Fujian, Peoples R China
基金
中国国家自然科学基金;
关键词
Uncaria rhynchophylla (UR); Angiotensin II; Hypertensive; Myocardial fibrosis; ROCK1; RHO-KINASE; THERAPEUTIC TARGET; CARDIAC FIBROSIS; HYPERTROPHY; PHYTOCHEMISTRY; CYTOSKELETON; PHARMACOLOGY; INHIBITION; CELLS;
D O I
10.1016/j.biopha.2021.112607
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Uncaria rhynchophylla (UR), a traditional Chinese medicine, has been proven effective in treating hypertensive patients in China. However, the mechanisms of action of UR in reducing hypertension and myocardial fibrosis are still unclear. The purpose of this study was to explore the role of UR in an angiotensin II (Ang II) induced mouse model. The mice were randomly divided into 5 groups and infused with Ang II (500 ng/kg/min) or saline, then administered UR (0.78, 1.56 or 3.12 g/kg/d) or saline for 4 weeks. UR treatment significantly attenuated the elevation of blood pressure caused by Ang II. It enhanced myocardial function and attenuated the increase in the heart weight index and the pathological changes in the Ang II-induced hypertensive mice. Furthermore, UR treatment inhibited cardiac fibrosis and significantly down-regulated collagen I, collagen III, and alpha-SMA protein expression in cardiac tissues. UR also attenuated the expression of RhoA, ROCK1, CTGF, and TGF-131. In cultured cardiac fibroblasts stimulated with Ang II, UR significantly down-regulated the expression of Collagen I, Collagen III, RhoA, ROCK1, and alpha-SMA. In summary, UR can significantly attenuate Ang II-induced hypertension and cardiac fibrosis, partly via suppression of the RhoA/ROCK1 signaling pathway.
引用
收藏
页数:10
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