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.