Sodium tanshinone IIA sulfate adjunct therapy reduces high-sensitivity C-reactive protein level in coronary artery

Siming Li1, Yang Jiao1,2, Hanjay Wang3

  • 1Cardiovascular Diseases Center, Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing, 100091, China.

Scientific Reports
|December 14, 2017
PubMed

Insights

Sodium tanshinone IIA sulfate (STS) effectively reduced high-sensitivity C-reactive protein (hs-CRP) and inflammation markers in coronary artery disease (CAD) patients. This adjunct therapy improved angina symptoms and offers a potential new treatment for cardiovascular inflammation.

Area of Science:

  • Cardiology
  • Pharmacology
  • Inflammation Research

Background:

  • High-sensitivity C-reactive protein (hs-CRP) is a key marker for cardiovascular events in coronary artery disease (CAD).
  • Reducing hs-CRP levels may offer additional benefits for CAD patients.

Purpose of the Study:

  • To evaluate the effectiveness of adjunct sodium tanshinone IIA sulfate (STS) therapy in reducing inflammation markers in CAD patients.
  • To assess the impact of STS on hs-CRP levels and angina symptoms.

Main Methods:

  • A parallel-design, randomized-controlled trial was conducted.
  • Patients with unstable angina or non-ST-elevation myocardial infarction and elevated hs-CRP were randomized.
  • The experimental group received standard therapy plus STS injection (80 mg daily for 14 days), while the control group received standard therapy alone.

Main Results:

  • The STS group showed significantly lower hs-CRP levels post-treatment (1.72 vs 3.20 mg/L, p=0.0191).
  • Adjunct STS therapy also reduced levels of interleukin-6, monocyte chemotactic protein-1 (MCP-1), and soluble CD40 ligand.
  • Improved angina symptom control and sustained lower MCP-1 levels were observed in the STS group post-treatment.

Conclusions:

  • Adjunct STS therapy, combined with standard medical care, effectively reduces elevated hs-CRP and other circulating inflammation markers in CAD patients.
  • STS demonstrates potential as an adjunctive treatment to improve inflammatory profiles and clinical outcomes in CAD.

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