Salvianolic Acid B-Alleviated Angiotensin II Induces Cardiac Fibrosis by Suppressing NF-κB Pathway In Vitro
Autor: | Chunhua Wang, Xiangchun Shen, Churui Chang, Hong Luo, Ling Tao, Yini Xu |
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Jazyk: | angličtina |
Rok vydání: | 2018 |
Předmět: |
0301 basic medicine
Cardiac fibrosis medicine.medical_treatment Salvia miltiorrhiza Collagen Type I Rats Sprague-Dawley 03 medical and health sciences 0302 clinical medicine Fibrosis Lab/In Vitro Research Cell Movement medicine Animals MTT assay Benzofurans Cell Proliferation biology Chemistry Growth factor Angiotensin II Myocardium NF-kappa B Heart General Medicine Fibroblasts medicine.disease Molecular biology Rats CTGF Fibronectin 030104 developmental biology 030220 oncology & carcinogenesis biology.protein I-kappa B Proteins |
Zdroj: | Medical Science Monitor : International Medical Journal of Experimental and Clinical Research |
ISSN: | 1643-3750 1234-1010 |
Popis: | BACKGROUND Salvianolic acid B (SalB) is the representative component of phenolic acids derived from the roots and rhizomes of Salvia miltiorrhiza Bge (Labiatae), which has been used widely in Asian countries for clinical therapy of various cardiovascular dysfunction-related diseases. However, cardiac protection effects and the underlying mechanism for clinical application are still poorly understood. Here, we investigated the potential anti-myocardial fibrosis effect and mechanism of SalB on Angiotensin II (Ang II)-induced cardiac fibrosis in vitro. MATERIAL AND METHODS The proliferation and migration capacity of cardiac fibroblasts (CFBs) were measured by MTT assay and scratch analysis, respectively. The colorimetric assay determined the hydroxyproline content in medium. Western blotting detected the protein expressions of nuclear transcription factor-kappa B (NF-κB) pathway-associated proteins, fibronectin (FN), collagen type I (Coll I), α-smooth muscle actin (α-SMA), and connective tissue growth factor (CTGF). The expression of α-SMA protein was observed by immunofluorescence staining. qRT-PCR detected the mRNA expression of NF-κB. RESULTS SalB attenuated Ang II-induced the proliferation and the migration ability of CFBs. Ang II-induced the extracellular matrix protein Coll I, FN, and α-SMA, the pro-fibrotic cytokine CTGF protein expression was inhibited, and the nuclear translocation of NF-κB p65 subunit was reduced by SalB. Western blotting and qRT-PCR confirmed that SalB blocked the activation of NF-κB induced by Ang II. PDTC (the NF-κB inhibitor) also inhibited proliferation of CFBs and reduced α-SMA and Coll I expression induced by Ang II. CONCLUSIONS SalB can alleviate Ang II-induced cardiac fibrosis via suppressing the NF-κB pathway in vitro. |
Databáze: | OpenAIRE |
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