Why the study?
Does Salvianolic acid B prevent cardiac remodeling in a rat model of myocardial infarction?
Does Salvianolic acid B prevent cardiac remodeling in a rat model of myocardial infarction?
Salvianolic acid B acts as a competitive inhibitor of MMP-9 and prevents adverse left ventricular remodeling in a rat model of myocardial infarction.
Answers are grounded in this paper and cite their sources.
Hypothesis-generating for SalB in post-MI remodeling; leaves open clinical translation pending human trials.
BACKGROUND: Infarct-induced left ventricular (LV) remodeling is a deleterious consequence after acute myocardial infarction (MI) which may further advance to congestive heart failure. Therefore, new therapeutic strategies to attenuate the effects of LV remodeling are urgently needed. Salvianolic acid B (SalB) from Salviae mitiorrhizae, which has been widely used in China for the treatment of cardiovascular diseases, is a potential candidate for therapeutic intervention of LV remodeling targeting matrix metalloproteinase-9 (MMP-9). RESULTS: Molecular modeling and LIGPLOT analysis revealed in silico docking of SalB at the catalytic site of MMP-9. Following this lead, we expressed truncated MMP-9 which contains only the catalytic domain, and used this active protein for in-gel gelatin zymography, enzymatic analysis, and SalB binding by Biacore. Data generated from these assays indicated that SalB functioned as a competitive inhibitor of MMP-9. In our rat model for cardiac remodeling, western blot, echocardiography, hemodynamic measurement and histopathological detection were used to detect the effects and mechanism of SalB on cardio-protection. Our results showed that in MI rat, SalB selectively inhibited MMP-9 activities without affecting MMP-9 expression while no effect of SalB was seen on MMP-2. Moreover, SalB treatment in MI rat could efficiently increase left ventricle wall thickness, improve heart contractility, and decrease heart fibrosis. CONCLUSIONS: As a competitive inhibitor of MMP-9, SalB presents significant effects on preventing LV structural damage and preserving cardiac function. Further studies to develop SalB and its analogues for their potential for cardioprotection in clinic are warranted.
No takes yet. Share an insight, caveat, or question.
Jiang et al. (2010) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: