机构：[1]Department of Cardiology, Tongren Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200336[2]Department of Cardiology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu 210029江苏省人民医院[3]Department of Internal Medicine, The Affiliated Drum Tower Hospital of Nanjing University Medical School, Nanjing, Jiangsu 210008[4]Department of General Practice, Tongren Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200336, P.R. China
Oxidative stress serves a key role in doxorubicin (DOX)-induced cardiotoxicity. The peptide Szeto-Schiller (SS)31 is an efficacious antioxidant with the capacity to reduce mitochondrial reactive oxygen species (ROS) levels and scavenge free radicals. Although SS31 is involved in the pathophysiological process of various cardiovascular diseases, the role of SS31 in DOX-induced cardiotoxicity remains unclear. To explore the effects of SS31 in DOX-induced cardiotoxicity, the present study first constructed DOX-induced cardiotoxicity models, in which H9c2 cells were incubated with 1 mu M DOX for 24 h and C57BL/6 mice were administered DOX (20 mg/kg cumulative dose). The results of various assays in these models demonstrated that SS31 exhibited a cardioprotective effect in vitro and in vivo by attenuating the level of ROS, stabilizing the mitochondrial membrane potential and ameliorating myocardial apoptosis as well as fibrosis following treatment with DOX. Mechanistically, the results of the present study revealed that the p38 MAPK signaling pathway was inhibited by SS31 in DOX-treated H9c2 cells, which was associated with the cardioprotective function of SS31. In addition, P79350, a selective agonist of p38 MAPK, reversed the protective effects of SS31. Taken together, these results demonstrated the effects of SS31 on ameliorating DOX-induced cardiotoxicity and indicated its potential as a drug for the treatment of DOX-induced cardiotoxicity.
基金：
National Natural Science Foundation of ChinaNational Natural Science Foundation of China (NSFC) [81570209, 81873540]; Key Clinical Frontier Technology Project of Department of Science and Technology of Jiangsu Provincial [BE2019752]
第一作者机构：[1]Department of Cardiology, Tongren Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200336[2]Department of Cardiology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu 210029
共同第一作者：
通讯作者：
通讯机构：[1]Department of Cardiology, Tongren Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200336[2]Department of Cardiology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu 210029[*1]Department of Cardiology, Tongren Hospital, Shanghai Jiao Tong University School of Medicine, 1111 Xianxia Road, Shanghai 200336, P.R. China[*2]Department of Cardiology, The First Affiliated Hospital of Nanjing Medical University, 300 Guangzhou Road, Nanjing, Jiangsu 210029, P.R. China
推荐引用方式(GB/T 7714)：
Zhang Li,Feng Mengwen,Wang Xuejun,et al.Peptide Szeto-Schiller 31 ameliorates doxorubicin-induced cardiotoxicity by inhibiting the activation of the p38 MAPK signaling pathway[J].INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE.2021,47(4):doi:10.3892/ijmm.2021.4896.
APA：
Zhang, Li,Feng, Mengwen,Wang, Xuejun,Zhang, Hao,Ding, Jingjing...&Qian, Lingmei.(2021).Peptide Szeto-Schiller 31 ameliorates doxorubicin-induced cardiotoxicity by inhibiting the activation of the p38 MAPK signaling pathway.INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE,47,(4)
MLA：
Zhang, Li,et al."Peptide Szeto-Schiller 31 ameliorates doxorubicin-induced cardiotoxicity by inhibiting the activation of the p38 MAPK signaling pathway".INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE 47..4(2021)
