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ERK/JNK 信号通路参与木犀草素对成年大鼠离体心脏缺血/再灌注损伤的保护作用
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ERK/JNK 信号通路参与木犀草素对成年大鼠离体心脏缺血/再灌注损伤的保护作用
吴鑫1,2,徐通达1,2,李东野1,2,陈秋平2,朱莎莎2
基金项目:基金项目:教育部2012 年高等学校博士学科专项科研基金(博导类联合,编号20123237110006)
作者简介:吴鑫(1988.10),女,硕士研究生,方向:心血管分子生物学
通信联系人:李东野(1954.04),男,教授,博导,研究方向:心血管分子生物学. 

 (1. 南京中医药大学第一临床学院,南京 210046;2. 江苏徐州医学院心血管病研究所,徐州 221002)
摘要:目的:观察木犀草素 (luteolin, Lut) 是否通过ERK1/2 及JNK 通路对缺血/再灌注(ischemia-reperfusion, I/R)成年大鼠离体心脏具有保护。方法:成年大鼠离体心脏分为以下几组:DMSO 组(DMSO, n=6),I/R 组(I/R, n=6),Lut 预处理组(Lut+I/R, n=6),PD98059预处理组(PD + I/R,n=6),PD98059 + Lut 预处理组(PD + Lut + I/R, n=6),SP600125预处理组(SP + I/R,n=6)。在I/R 过程中检测血流动力学指标。各组复灌10min 时,留取冠脉液测LDH 含量,冷冻心脏,测量各组心脏的心肌梗死面积。各组实验完毕后甲醛固定心肌,用于TUNEL 检测心肌细胞的凋亡。结果:在离体器官水平上,与正常组相比较,I/R组能够明显地降低离心脏功能的各种参数,促进冠脉流出液中LDH 的释放量,增加心肌梗死面积。Lut 及JNK 抑制剂SP 预处理可部分逆转上述指标的变换;而ERK1/2 抑制剂 PD在Lut 预处理之前干预后,Lut 的保护作用可部分被阻断,而单独用PD 预处理相对于I/R
组上述指标未见明显的变化。结论:Lut 及JNK 抑制剂SP 可改善I/R 大鼠离体心脏收缩功能,减少灌流液中LDH 的量,抑制心肌细胞的凋亡,改善心肌的梗死面积。
关键词:木犀草素;缺血/再灌注;心肌收缩功能;ERK1/2;JNK
中图分类号:R5
ERK1/2 and JNK pathways are involved in luteolin mediated protection of rat hearts following ischemia/reperfusion
WU Xin1,2, XU Tongda1,2, LI Dongye1,2, CHEN Qiuping2, ZHU Shasha2
(1. The First Clinical College, Nanjing Traditional Chinese Medicine University, Nanjing, Jiangsu 210046;2. Research Institute of Cardiovascular Diseases, Xuzhou Medical College, Xuzhou, Jiangsu 221002)
Abstract: Objective: In order to detect if luteolin through ERK1/2 and JNK pathways resistance to damages of rat hearts during ischemia-reperfusion (I/R) process. Methods:Isolating heart of adult rat, then in the organ level the rats were randomly repartitioned into the following groups,including DMSO (DMSO, n=6), ischemia-reperfusion group (I/R, n=6), luteolin pretreatment group (Lut + I/R, n=6), PD98059 pretreatment group (PD + I/R, n=6), luteolin plus PD98059
35 pretreatment group (PD + Lut + I/R, n=6), and JNK inhibitor SP600125 pretreatment group (SP +I/R, n=6). Left ventricular shrink and diastole function was continuously monitored before and during the entire I/R procedure. The coronary effluent of each group was collected after 10-minute reperfusion for determination of lactate dehydrogenase (LDH) activity, all the hearts were frozen for measure infarct size, and formaldhyde fixed myocardial for TUNEL detection of cell apoptosis.
Results: In vitro organ level, compared to DMSO group, I/R can clearly deceased all heart function parameters, increased infarct size and the release of LDH. However, pretreatment with luteolin or SP600125 before I/R can effectively improved cardiac systolic/diastolic function,decreased LDH release and infarct size, butalone treatment with PD98059 haven’t the effect.

Administration of PD98059 before luteolin markedly reversed the beneficial effect of luteolin on these parameters of myocardial function. Conclusion:  Luteolin and JNK inhibitor of SP600125 could improves contractile function of rat heart, reduce the release of LDH in perfusion liquid,
inhibit the apoptosis of myocardial cells, and decrease the infarction area of heart.
Key words: Luteolin ; ischemia/reperfusion ; contraction function ; ERK1/2 5; JNK