首页
期刊简介
编 委 会
期刊订阅
百年学会 医星璀璨
名院风范
学科风华
菁英风采
投稿须知
过刊浏览
联系我们
篇名
关键词
作者
作者单位
摘要
关键词
注册本刊作者
作者投稿查稿
专家远程审稿
编辑在线审稿
编务办公专区
主编办公专区
下载文档
《上海医学》审稿费代缴委托书
《上海医学》杂志2024年征订启事
《上海医学》期刊编审系统审稿专家使用手册
工作动态
03-05
《上海医学》杂志2024年度“春蕾杯”论文评比征文通知
06-14
创新驱动,培育人才—《上海医学》2021年度春蕾计划评审结果揭晓
01-21
《上海医学》期刊影响力指标和学科排名取得显著提升
01-20
《上海医学》恭祝大家新年快乐!
08-18
作废声明
联系方式
发行周期:
月刊
主管单位:
上海市卫生健康委员会
主办单位:
上海市医学会
编辑出版:
《上海医学》编辑部
联系地址:
上海市北京西路1623号
邮编:
200040
电话:
021-62178606
传真:
021-62178606
邮箱:
smasmj@shsma.org.cn
ISSN:
ISSN0253-9934
CN:
CN31-1366/R
收款账号:
1001255309008900719
账户名:
上海市医学会
开户行:
工商银行上海市静安寺支行
友情链接
上海市医学会
当前位置:首页 >
二氮嗪后处理对大鼠缺血再灌注心肌损伤和糖原合成酶激酶-3β表达的影响
Effects of diazoxide-postconditioning on myocardial ischemia reperfusion injury and the expression of glycogen synthase kinase-3β in rats
浏览(593) 下载(0)
DOI:
作者:
赵其宏,张颖,栾恒飞,叶英,曾因明
ZHAO Qihong, ZHANG Ying, LUAN Hengfei, YE Ying, ZENG Yinming
作者单位:
蚌埠医学院第一附属医院
Department of Anesthesiology, The First Affiliated Hospital, Bengbu Medical College, Bengbu, 233004, Anhui, China
关键词:
心肌再灌注损伤;二氮嗪;1-磷脂酰肌醇3-激酶;蛋白质丝氨酸苏氨酸激酶;糖原合成酶激酶-3β
Myocardial reperfusion injury; Diazoxide; 1-Phosphatidylinositol 3-kinase; Protein serine threonine kinase; Glycogen synthase kinase-3β
摘要:
【摘要】 目的 研究磷脂酰肌醇-3-激酶/蛋白质丝氨酸苏氨酸激酶(PI3K/ Akt)信号通路对二氮嗪后处理大鼠缺血再灌注(I/R)心肌保护作用的影响及机制。方法 60只雄性SD大鼠随机分为五组:假手术组(Sham组)、I/R组、二氮嗪7 mg﹒kg-1组(D组)、渥蔓菁霉素15 μg﹒kg-1组(W组)和二氮嗪+渥蔓菁霉素组(D+W组)。结扎左冠状动脉前降支30 min、再开放120 min建立心肌I/R损伤模型。再灌注末,比色法检测血浆乳酸脱氢酶(LDH)、肌酸激酶(CK)活性,电镜观察心肌超微结构变化,比色法测量心肌组织内半胱氨酸天冬氨酸特异性蛋白酶-3(Caspase-3)活性, western blot测定糖原合成酶激酶-3β(GSK-3β)和磷酸化GSK-3β(p-GSK-3β)的表达。结果 与I/R组相比,D组和D+W组LDH和CK活性显著降低(P<0.01),心肌超微结构改变减轻,Caspase-3活性降低(P<0.01),p-GSK-3β表达增加(P<0.01)。与D组相比,D+W组LDH和CK活性显著增高(P<0.05),心肌超微结构损伤严重,Caspase-3活性增加(P<0.05),p-GSK-3β表达降低(P<0.01)。结论 二氮嗪后处理通过激活PI3K/Akt信号通路减轻大鼠心肌I/R损伤的机制与p-GSK-3β的表达增加有关。
【Abstract】 Objective To study effects of the phosphatidylinositol 3- kinase / protein serine threonine kinase (PI3K/Akt) signal pathway in cardioprotection induced by diazoxide-postconditioning against ischemia reperfusion (I/R) and its potential mechanism in rats. Methods 60 male SD rats were randomly divided into five groups: sham operation (Sham), I/R, diazoxide 7 mg﹒kg-1 (D), wortmannin 15 μg﹒kg-1 (W) and diazoxide + wortmannin (D+W) group. Myocardial I/R injury model was established by ligation of left anterior descending coronary artery 30 min followed by reperfusion for 120 min. At the end of reperfusion, lactate dehydrogenase (LDH) and creatine kinase (CK) in plasma were measured by colorimetric measurement, myocardial ultrastructure changes were examined by electron microscope, the activity of cysteinyl aspartate specific protease3 (Caspase-3) in myocardium was detected, and the expression of glycogen synthase kinase-3β (GSK-3β) and phosphorylation of GSK-3β (p-GSK-β) was measured by western blot. Results Compared with I/R group, LDH and CK in plasma were all significantly decreased (P<0.01), myocardial ultrastructure changes more slightly, Caspase-3 activity were decreased markedly (P<0.01), and the expression of p-GSK-3β were increased significantly (P<0.01) in D and D+W group. Compared with D group, LDH and CK in plasma were all significantly increased (P<0.05), myocardial ultrastructural changes more severity, Caspase-3 activity was increased (P<0.05), the expression of p-GSK-3β was decreased significantly (P<0.01) in D+W group. Conclusion PI3K/Akt signaling pathway participates in diazoxide-postconditioning to attenuate rat myocardial I/R injury through up-regulation the expression of p-GSK-3β.
点击下载DOC全文