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Iranian Journal of Basic Medical Sciences، جلد ۲۷، شماره ۱، صفحات ۱۰۷-۱۱۳
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عنوان انگلیسی Effects of ivabradine on myocardial autophagia and apoptosis in isoprenaline-induced heart failure in mice
چکیده انگلیسی مقاله Objective(s): To investigate the effects and mechanisms of ivabradine (IVA) on isoprenaline-induced cardiac injury.Materials and Methods: Forty male C57BL/6 mice were randomly divided into control group, model group, high-dose IVA group, and low-dose IVA group. The control group was given saline, other groups were given subcutaneous injections of isoproterenol (ISO) 5 mg/kg/d to make the myocardial remodeling model. A corresponding dose of IVA (high dose 50 mg/kg/d, low dose 10 mg/kg/d) was given by gavage (30 days). A transthoracic echocardiogram was obtained to detect the structure and function of the heart. An electron microscope was used to explore the cardiomyocytes’ apoptosis and autophagy. HE staining and Masson’s trichrome staining were performed to explore myocardial hypertrophy and fibrosis. Western blot was used to detect Bax, Bcl-2, cleaved caspase-3, Becline-1, LC3, phosphorylated p38 mitogen-activated protein kinase (p-p38MAPK), phosphorylated extracellular regulated protein kinases1/2 (p-ERK1/2), phosphorylated c-Jun N-terminal kinase (p-JNK), and α-smooth muscle actin (α-SMA) in the myocardium.Results: Heart rate in the IVA groups was reduced, and the trend of heart rate reduction was more obvious in the high-dose group. Echocardiography showed that IVA improved the cardiac structure and function compared to the model group. IVA attenuated cardiac fibrosis, decreased cardiomyocyte apoptosis, and increased autophagy. The phosphorylated MAPK in the ISO-induced groups was increased. IVA treatment decreased the p-p38MAPK level. There were no differences in p-ERK and p-JNK levels.Conclusion: The beneficial effects of IVA on myocardial injury are related to blocking the p38MAPK signal pathway, decreasing cardiomyocyte apoptosis, and increasing cardiomyocyte autophagy.
کلیدواژه‌های انگلیسی مقاله Apoptosis, Autophagy, Cardiac remodeling, Fibrosis, heart failure
نویسندگان مقاله | Menghua Sun
Department of Cardiology, Fourth Affiliated Hospital of Harbin Medical University, Harbin 150001, China


| Feiya Yin
The University of Sydney, Newtown, NSW 2042, Australia


| Xinrong Wu
Department of Cardiology, Fourth Affiliated Hospital of Harbin Medical University, Harbin 150001, China


| Shaoer Sun
Department of Geriatric Cardiology, Guangdong Provincial People’s Hospital, Guangzhou, PR. China, 510080


| Yongqiang An
Department of Cardiology, Fourth Affiliated Hospital of Harbin Medical University, Harbin 150001, China


| Manlin Zhu
Department of Cardiology, Fourth Affiliated Hospital of Harbin Medical University, Harbin 150001, China


| Xiaomin Li
Department of Cardiology, Fourth Affiliated Hospital of Harbin Medical University, Harbin 150001, China


| Wei Liu
Department of Cardiology, Fourth Affiliated Hospital of Harbin Medical University, Harbin 150001, China
نشانی اینترنتی https://ijbms.mums.ac.ir/article_23140.html
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