Title:Sodium Tanshinone IIA Sulfonate Improves Adverse Ventricular Remodeling
Post-MI by Reducing Myocardial Necrosis, Modulating Inflammation, and Promoting
Angiogenesis
Volume: 28
Issue: 9
Author(s): Baoli Zhang, Peng Yu, Enyong Su, Jianguo Jia, Chunyu Zhang, Shiyao Xie, Zhenhui Huang, Ying Dong, Jinguo Ding, Yunzeng Zou, Hong Jiang*Junbo Ge
Affiliation:
- Department of Cardiology, Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai
200032, China
Keywords:
Sodium tanshinone IIA sulfonate, myocardial infarction, cardiac function, cardiac remodeling, necrosis, inflammation, angiogenesis.
Abstract:
Background and Objective: Myocardial infarction (MI) leads to pathological cardiac remodeling
and heart failure. Sodium tanshinone IIA sulfonate (STS) shows to possess therapeutic potential. The present
study aimed to explore the potential role of STS in ventricular remodeling post-MI.
Methods: Mice were randomly divided into sham, MI + normal saline (NS) and MI + STS (20.8 mg/kg/day intraperitoneally)
groups. MI was established following left anterior descending artery ligation. Cardiac function
was evaluated using echocardiography. Scar size and myocardial fibrosis-associated markers were detected using
Masson’s trichrome staining and western blot analysis (WB). Necrosis and inflammation were assessed using
H&E staining, lactate dehydrogenase (LDH) detection, ELISA, immunohistochemical staining, and WB.
Furthermore, angiogenesis markers and associated proteins were detected using immunohistochemical staining
and WB.
Results: Mice treated with STS exhibited significant improvements in cardiac function, smaller scar size, and
low expression levels of α-smooth muscle actin and collagen I and III at 28 days following surgery, compared
with the NS-treated group. Moreover, treatment with STS reduced eosinophil necrosis, the infiltration of inflammatory
cells, plasma levels of LDH, high mobility group protein B1, interleukin-1β and tumor necrosis factor-
α, and protein expression of these cytokines at 3 days. Macrophage infiltration was also decreased in the
STS group in the early phase. Additionally, CD31+ vascular density, protein levels of hypoxia-inducible factor-
1α, and vascular endothelial growth factor were elevated in the STS-treated mice at 28 days.
Conclusion: STS improved pathological remodeling post-MI, and the associated therapeutic effects may be a
result of a decrease in myocardial necrosis, modulation of inflammation, and an increase in angiogenesis.
