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ERK/JNK 信號通路參與木犀草素對成年大鼠離體心臟缺血/再灌注損傷的保護作用
來源: | 作者: | 發布時間:2014-4-15 15:01:28

ERK/JNK 信號通路參與木犀草素對成年大鼠離體心臟缺血/再灌注損傷的保護作用
吳鑫1,2,徐通達1,2,李東野1,2,陳秋平2,朱莎莎2
基金項目:基金項目:教育部2012 年高等學校博士學科專項科研基金(博導類聯合,編號20123237110006)
作者簡介:吳鑫(1988.10),女,碩士研究生,方向:心血管分子生物學
通信聯系人:李東野(1954.04),男,教授,博導,研究方向:心血管分子生物學. 

 (1. 南京中醫藥大學第一臨床學院,南京 210046;2. 江蘇徐州醫學院心血管病研究所,徐州 221002)
摘要:目的:觀察木犀草素 (luteolin, Lut) 是否通過ERK1/2 及JNK 通路對缺血/再灌注(ischemia-reperfusion, I/R)成年大鼠離體心臟具有保護。方法:成年大鼠離體心臟分為以下幾組:DMSO 組(DMSO, n=6),I/R 組(I/R, n=6),Lut 預處理組(Lut+I/R, n=6),PD98059預處理組(PD + I/R,n=6),PD98059 + Lut 預處理組(PD + Lut + I/R, n=6),SP600125預處理組(SP + I/R,n=6)。在I/R 過程中檢測血流動力學指標。各組復灌10min 時,留取冠脈液測LDH 含量,冷凍心臟,測量各組心臟的心肌梗死面積。各組實驗完畢后甲醛固定心肌,用于TUNEL 檢測心肌細胞的凋亡。結果:在離體器官水平上,與正常組相比較,I/R組能夠明顯地降低離心臟功能的各種參數,促進冠脈流出液中LDH 的釋放量,增加心肌梗死面積。Lut 及JNK 抑制劑SP 預處理可部分逆轉上述指標的變換;而ERK1/2 抑制劑 PD在Lut 預處理之前干預后,Lut 的保護作用可部分被阻斷,而單獨用PD 預處理相對于I/R
組上述指標未見明顯的變化。結論:Lut 及JNK 抑制劑SP 可改善I/R 大鼠離體心臟收縮功能,減少灌流液中LDH 的量,抑制心肌細胞的凋亡,改善心肌的梗死面積。
關鍵詞:木犀草素;缺血/再灌注;心肌收縮功能;ERK1/2;JNK
中圖分類號: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

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