Shenfu injection attenuates lipopolysaccharide-induced myocardial inflammation and apoptosis in rats

作     者：CHEN Rui-Juan RUI Qing-Lin WANG Qiong TIAN Fang WU Jian KONG Xiang-Qing CHEN Rui-Juan;RUI Qing-Lin;WANG Qiong;TIAN Fang;WU Jian;KONG Xiang-Qing

作者机构：Cardiology Departmentthe First Affiliated Hospital with Nanjing Medical UniversityNanjing 210029China Emergency DepartmentAffiliated Hospital of Nanjing University of Chinese MedicineJiangsu Province Hospital of Chinese MedicineNanjing 210029China Clinical Pharmacology DepartmentAffiliated Hospital of Nanjing University of Chinese MedicineJiangsu Province Hospital of Chinese MedicineNanjing 210029China Central LaboratoryAffiliated Hospital of Nanjing University of Chinese MedicineJiangsu Province Hospital of Chinese MedicineNanjing 210029China 

出 版 物：《Chinese Journal of Natural Medicines》 (中国天然药物（英文版）)

年 卷 期：2020年第18卷第3期

页      面：226-233页

核心收录：

学科分类：0710[理学-生物学] 1007[医学-药学(可授医学、理学学位)] 1006[医学-中西医结合] 1005[医学-中医学] 1002[医学-临床医学] 0703[理学-化学] 10[医学] 100602[医学-中西医结合临床] 

主　　题：Shenfu injection Lipopolysaccharide Inflammation Apoptosis Mitogen-activated protein kinase kinase Extracellular regulated protein kinases 

摘      要：Shenfu injection(SFI), a Chinese medicinal product, shows potent efficacy in treating sepsis. The aim of the present study was to clarify the protective effects of SFI against lipopolysaccharide(LPS)-induced myocardial inflammation and apoptosis.Experiments were carried out in Sprague-Dawley(SD) rats treated with LPS or LPS + SFI, and in H9 C2 cardiomyocytes. The sepsisassociated myocardial inflammation and apoptosis was induced by the intraperitoneal injection of LPS(20 mg·kg–1). SFI attenuated the increased expression of tumor necrosis factor(TNF)-α and interleukin(IL)-1β induced by LPS both in serum and heart. In LPS group,cell viability was reduced, and reversed after SFI administration. LPS treatment increased the expression levels of cleaved-caspase 3 and Bax, and those of Bcl2 and Bcl2/Bax. These two trends were reversed by SFI administration. The expression levels of phosphorylated mitogen-activated protein kinase kinase(p-MEK) and phosphorylated extracellular regulated protein kinases(p-ERK) were increased by LPS, and reversed by SFI. MEK inhibitor U0126 attenuated the apoptosis induced by LPS. These results indicate that SFI could treat LPS-induced cardiac dysfunction. In conclusion, SFI attenuates the inflammation and apoptosis induced by LPS via downregulating the MEK and ERK signaling pathways.