Salvianolic acid A protects against myocardial ischemia/reperfusion injury by reducing platelet activation and inflammation

Yuan,Xiaoling; Xiang,Yijia; Zhu,Ning; Zhao,Xuyong; Ye,Shiyong; Zhong,Peng; Zeng,Chunlai

doi:10.3892/etm.2017.4619

Salvianolic acid A protects against myocardial ischemia/reperfusion injury by reducing platelet activation and inflammation

Authors:
- Xiaoling Yuan
- Yijia Xiang
- Ning Zhu
- Xuyong Zhao
- Shiyong Ye
- Peng Zhong
- Chunlai Zeng
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Affiliations: Department of Cardiology, The Fifth Affiliated Hospital of Wenzhou Medical University, Lishui, Zhejiang 323000, P.R. China
Published online on: June 15, 2017 https://doi.org/10.3892/etm.2017.4619
Pages: 961-966
Copyright: © Yuan et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

The aim of the present study was to investigate the protective effect of salvianolic acid A (SAA) on myocardial ischemia/reperfusion injury in rats. SAA (10 mg/kg) or Tirofiban (60 µg/kg) was administered to rats by jugular vein injection 10 min before the initiation of reperfusion. After 3 h of reperfusion, platelet aggregation was measured using an aggregometer and levels of nitric oxide (NO) were detected using an ultraviolet spectrophotometer. Serum levels of cardiac troponin T (cTnT), creatine kinase isoenzyme MB (CK‑MB), p‑selectin, interleukin‑1β (IL‑1β) and tumor necrosis factor‑α (TNF‑α) were also measured 3 and 24 h after reperfusion. Furthermore, morphology of the ischemic myocardium was histopathologically analyzed by hematoxylin and eosin staining, and the infarct area was evaluated by Evans blue and triphenyltetrazolium chloride staining. In rats subjected to reperfusion, it was observed that pretreatment with SAA significantly increased the survival rate (P<0.05), and that increased survival rate was due to a significant decrease in infarct size, as evidenced by significantly reduced serum levels of cTnT and CK‑MB (P<0.05). In addition, decreases in infarct size occurred through the inhibition of platelet aggregation and inflammation associated with reperfusion‑induced myocardial cell damage, as indicated by reduced serum levels of p‑selectin, TNF‑α, IL‑1β and NO. In conclusion, SAA was protective against myocardial ischemia/reperfusion injury in rats by serving antiplatelet and anti‑inflammation roles.

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