Chemical Mechanisms of Sodium Tanshinone IIA Sulfonate in Modulating SIRT1-Mediated Inflammation and Oxidative Stress
نویسندگان
1 Department of Cardiology, Affiliated Nanjing Brain Hospital, Nanjing Medical University, Nanjing, Jiangsu, 210029, P.R. CHINA
2 Department of Cardiology, Affiliated Nanjing Brain Hospital, Nanjing Medical University, Nanjing, Jiangsu, 210029, P.R. CHINA
3 Department of Cardiology, Affiliated Nanjing Brain Hospital, Nanjing Medical University, Nanjing, Jiangsu, 210029, P.R. CHINA
4 Department of Cardiology, Affiliated Nanjing Brain Hospital, Nanjing Medical University, Nanjing, Jiangsu, 210029, P.R. CHINA
5 Department of Cardiology, Affiliated Nanjing Brain Hospital, Nanjing Medical University, Nanjing, Jiangsu, 210029, P.R. CHINA
6 Department of Cardiology, Affiliated Nanjing Brain Hospital, Nanjing Medical University, Nanjing, Jiangsu, 210029, P.R. CHINA
7 Department of Cardiology, Affiliated Nanjing Brain Hospital, Nanjing Medical University, Nanjing, Jiangsu, 210029, P.R. CHINA
doi
10.30492/ijcce.2025.2065781.7198چکیده
Sodium Tanshinone IIA Sulfonate (STS), a sulfonated derivative of tanshinone IIA with the molecular formula C19H17NaO6S and a molecular weight of 396.69 g/mol, exhibits significant anti-inflammatory and antioxidant properties due to its sulfonate group, which enhances water solubility and bioavailability. This study investigated the chemical mechanisms of STS in Coronary Heart Disease (CHD) via SIRT1-mediated pathways. First of all, the CHD rat model was established by left coronary artery ligation combined with ischemia/reperfusion injury. The rats were randomly divided into control, model, low (10 mg/kg), medium (20 mg/kg), and high (40 mg/kg) dose STS groups, with chemical purity >98%. Liver function test was used to determine the optimal dose of STS intervention (20 mg kg), Western blot (WB) was used to detect the expression of SIRT1 protein, tissue staining (HE, oil red O) was used to observe the atherosclerotic lesions, and cardiac function was evaluated by a cardiac function instrument. Results showed STS dose-dependently upregulates SIRT1 expression (P<0.05), reduces atherosclerotic plaque formation (oil red O staining), and improves hemodynamics by modulating NF-κB and Nrf2 pathways. STS at 20 mg/kg demonstrated optimal efficacy with minimal hepatotoxicity. These findings highlight STS's role in regulating inflammation and oxidative stress via SIRT1, providing a basis for its use in cardiovascular therapy.
