Yun Pan - Department of Emergency, The First Affiliated Hospital, Soochow University, ۱۸۸ Shi-Zi Road, Suzhou ۲۱۵۰۰۶, PR China
Jin-Xian Qian - Department of Emergency, Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou Municipal Hospital, Suzhou, P.R. China
Shi-Qi Lu - Department of Emergency, The First Affiliated Hospital, Soochow University, ۱۸۸ Shi-Zi Road, Suzhou ۲۱۵۰۰۶, PR China
Jing-Wei Chen - Department of Internal Medicine, The Affiliated Suzhou Chinese Traditional Medicine Hospital, Nanjing University of Chinese Medicine, Yang-Su Road, Suzhou ۲۱۵۰۰۳, P.R. China
Xiao-Dong Zhao - Department of Internal Medicine, The Affiliated Suzhou Chinese Traditional Medicine Hospital, Nanjing University of Chinese Medicine, Yang-Su Road, Suzhou ۲۱۵۰۰۳, P.R. China
Yan Jiang - Department of Physiology, Medical College of Soochow University, ۱۹۹ Ren-Ai Road, Dushu Lake Campus, Suzhou Industrial Park, Suzhou ۲۱۵۱۲۳, P.R. China
Lin-Hui Wang - Department of Physiology, Medical College of Soochow University, ۱۹۹ Ren-Ai Road, Dushu Lake Campus, Suzhou Industrial Park, Suzhou ۲۱۵۱۲۳, P.R. China
Guo-Xing Zhang - Department of Physiology, Medical College of Soochow University, ۱۹۹ Ren-Ai Road, Dushu Lake Campus, Suzhou Industrial Park, Suzhou ۲۱۵۱۲۳, P.R. China

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 ۳۰-min coronary arterial occlusion followed by ۲۴ hours' reperfusion. Half an hour before the left coronary artery ligation, rats were pretreated with TSS in three different dosages (۱۵, ۳۰, ۷۰ 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 box۱ (HMGB-۱), anti-apoptotic protein Bcl-۲, pro-apoptotic mediators such as Bax and Caspase-۳, markers of autophagy such as ratio of LC۳B/LC۳A and Beclin-۱ expression. Results: Our results showed that TSS dose-dependently improves cardiac function, accompanied with decrease of HMGB۱ level, increase of LC۳B/LC۳A ratio and increase of Beclin-۱ expression. TSS treatment down-regulates Bax and Caspase-۳ expression, while up-regulating Bcl-۲ levels. Conclusion: TSS ameliorates I/R induced myocardial injury and improves cardiac function via reducing inflammation and apoptosis, while enhancing autophagy.

Apoptosis, Autophagy, Ischemia/reperfusion (I/R), Tanshinone IIA sodium-sulfonate (TSS)