Protective effects of polygalasaponin F on oxidative stress and apoptosis-induced ischemic myocardial injury in neonatal rats with hypoxic-ischemic brain damage

被引:10
作者
Zhou, Wen-Li [1 ]
Zhang, Jian-Tao [2 ]
Xu, Wei [1 ]
Sun, Jing-Hui [1 ]
机构
[1] First Hosp Jilin Univ, Dept Pediat, 71 Xinmin Rd, Changchun 130000, Jilin, Peoples R China
[2] First Hosp Jilin Univ, Dept Anocolorectal Surg, Changchun, Jilin, Peoples R China
关键词
apoptosis; hypoxic-ischemic brain damage; myocardial injury; oxidative stress; polygalasaponin F; DYSFUNCTION; PATHWAY;
D O I
10.1097/WNR.0000000000001330
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
The aim of the present study was to evaluate the role of polygalasaponin F on ischemic myocardial injury in neonatal rats with hypoxic-ischemic brain damage. A primary in-vitro myocardial cell oxygen-glucose deprivation/reperfusion model and an in-vivo middle cerebral artery occlusion model were established. The results demonstrated that polygalasaponin F protects myocardium in hypoxic-ischemic brain injury. The mechanisms of its protective effect involved in (1) reducing oxidant stress injury, (2) reducing the apoptosis rate of myocardial cells through increasing the Bcl-2 protein level and decreasing the Cyt-C and Bax values, and (3) alleviating liver and kidney damage caused by cerebral hypoxia and ischemia via reducing the damage markers. The results of the present study may contribute toward the development of novel strategies for clinical cardioprotection with hypoxic-ischemic brain damage. Copyright (C) 2019 Wolters Kluwer Health, Inc. All rights reserved.
引用
收藏
页码:1148 / 1156
页数:9
相关论文
共 25 条
[1]  
Ashok G, 2011, J Assoc Physicians India, V59, P737
[2]   Vulnerability of the developing brain to hypoxic-ischemic damage: contribution of the cerebral vasculature to injury and repair? [J].
Baburamani, Ana A. ;
Ek, C. Joakim ;
Walker, David W. ;
Castillo-Melendez, Margie .
FRONTIERS IN PHYSIOLOGY, 2012, 3
[3]   Blood Urea Nitrogen/Creatinine Ratio Identifies a High-Risk but Potentially Reversible Form of Renal Dysfunction in Patients With Decompensated Heart Failure [J].
Brisco, Meredith A. ;
Coca, Steven G. ;
Chen, Jennifer ;
Owens, Anjali Tiku ;
McCauley, Brian D. ;
Kimmel, Stephen E. ;
Testani, Jeffrey M. .
CIRCULATION-HEART FAILURE, 2013, 6 (02) :233-239
[4]   Hepatic Dysfunction in Asphyxiated Neonates: Prospective Case-Controlled Study [J].
Choudhary, Mukesh ;
Sharma, Deepak ;
Dabi, Dhanraj ;
Lamba, Mamta ;
Pandita, Aakash ;
Shastri, Sweta .
CLINICAL MEDICINE INSIGHTS-PEDIATRICS, 2015, 9 :1-6
[5]   Oxygen Free Radicals and Excitation-Contraction Coupling [J].
Goldhaber, Joshua I. ;
Qayyum, Mohammed S. .
ANTIOXIDANTS & REDOX SIGNALING, 2000, 2 (01) :55-64
[6]  
Gupta BD, 2005, INDIAN PEDIATR, V42, P928
[7]   Preferential Cephalic Redistribution of Left Ventricular Cardiac Output during Therapeutic Hypothermia for Perinatal Hypoxic-Ischemic Encephalopathy [J].
Hochwald, Ori ;
Jabr, Mohammad ;
Osiovich, Horacio ;
Miller, Steven P. ;
McNamara, Patrick J. ;
Lavoie, Pascal M. .
JOURNAL OF PEDIATRICS, 2014, 164 (05) :999-+
[8]   BCL-2 FUNCTIONS IN AN ANTIOXIDANT PATHWAY TO PREVENT APOPTOSIS [J].
HOCKENBERY, DM ;
OLTVAI, ZN ;
YIN, XM ;
MILLIMAN, CL ;
KORSMEYER, SJ .
CELL, 1993, 75 (02) :241-251
[9]   Epidemiology of neonatal encephalopathy and hypoxic-ischaemic encephalopathy [J].
Kurinczuk, Jennifer J. ;
White-Koning, Melanie ;
Badawi, Nadia .
EARLY HUMAN DEVELOPMENT, 2010, 86 (06) :329-338
[10]  
Lee C-T, 2018, COMPLEMENTARY THERAP, DOI [10.5772/intechopen.76373, DOI 10.5772/INTECHOPEN.76373]