Author/Authors :
Pan، Yun نويسنده First Affiliated Hospital,Department of Emergency,Soochow University,Suzhou,China , , Qian، Jin-Xian نويسنده Suzhou Municipal Hospital,Department of Emergency,Affiliated Suzhou Hospital of Nanjing Medical University,Suzhou,,China , , Lu، Shi-Qi نويسنده First Affiliated Hospital,Department of Emergency,Soochow University,Suzhou,China , , Chen، Jing-Wei نويسنده Affiliated Suzhou Chinese Traditional Medicine Hospital,Department of Internal Medicine,Nanjing University of Chinese Medicine,Suzhou,China , , Zhao، Xiao-Dong نويسنده Affiliated Suzhou Chinese Traditional Medicine Hospital,Department of Internal Medicine,Nanjing University of Chinese Medicine,Suzhou,China , , Jiang، Yan نويسنده Medical College,Department of Physiology,Soochow University, Dushu Lake Campus,Suzhou,China , , Wang، Lin-Hui نويسنده Medical College,Department of Physiology,Soochow University, Dushu Lake Campus,Suzhou,China , , Zhang، Guo-Xing نويسنده Medical College,Department of Physiology,Soochow University, Dushu Lake Campus,Suzhou,China ,
Abstract :
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.
