Protective effects of tanshinone IIA sodium sulfonate on ischemia-reperfusion-induced myocardial injury in rats

• Main Authors: Yun Pan, Jin-Xian Qian, Shi-Qi Lu, Jing-Wei Chen, Xiao-Dong Zhao, Yan Jiang, Lin-Hui Wang, Guo-Xing Zhang
• Format: Article
• Language: English
• Published: Mashhad University of Medical Sciences 2017-03-01
• Series: Iranian Journal of Basic Medical Sciences
• Subjects: Apoptosis; Autophagy; Ischemia/reperfusion (I/R); Tanshinone IIA sodium-sulfonate (TSS)
• Online Access: http://ijbms.mums.ac.ir/article_8361_d49cca63ad0e992964747456edf2563c.pdf

Objective(s): This study investigated the protective effect of tanshinone IIA sodium sulfonate (TSS) on ischemia-reperfusion (I/R) induced cardiac injury, and the underlying mechanism of action. Materials and Methods:Male Sprague-Dawley rats were subjected to a 30-min coronary arterial occlusion followed by 24 hours' reperfusion. Half an hour before the left coronary artery ligation, rats were pretreated with TSS in three different dosages (15, 30, 70 mg/kg, IP). Twenty-four hours later, cardiac function was measured and the ratio of infarct size to area at risk (AAR) was calculated. Western blotting examined the expression of the inflammatory mediator high-mobility group box1 (HMGB-1), anti-apoptotic protein Bcl-2, pro-apoptotic mediators such as Bax and Caspase-3, markers of autophagy such as ratio of LC3B/LC3A and Beclin-1 expression. Results: Our results showed that TSS dose-dependently improves cardiac function, accompanied with decrease of HMGB1 level, increase of LC3B/LC3A ratio and increase of Beclin-1 expression. TSS treatment down-regulates Bax and Caspase-3 expression, while up-regulating Bcl-2 levels. Conclusion: TSS ameliorates I/R induced myocardial injury and improves cardiac function via reducing inflammation and apoptosis, while enhancing autophagy.