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川芎嗪对再灌注大鼠心肌细胞c-fos基因表达及凋亡的影响(PDF)

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2000年第3期
页码:
213-215
栏目:
论著
出版日期:
2000-05-25

文章信息/Info

Title:
Effects of tetramethylpyrazine on c-fos expression and apoptosis of myocardial cells in myocardial ischemic reperfusion in rats
作者:
李源 段红 王天成 张珊红 龚卫琴
第四军医大学西京医院老年病科, 陕西西安710033
Author(s):
LI Yuan DUAN Hong WANG Tian-cheng ZHANG Shan-hong GONG Wei-qin
Department of Geriatrics, Xijing Hospital, Fourth Military Medical University, Xi′an 710033,Shaanxi,China
关键词:
心肌缺血再灌注c-fos基因细胞调亡川芎嗪
Keywords:
myocardial ischemic reperfusionc-fos expressionapoptosistetramethylpyrazine
分类号:
R331.31
DOI:
-
文献标识码:
A
摘要:
目的 观察川芎嗪(TMP)对心肌缺血再灌注(MIR)大鼠心肌c-fos基因表达及凋亡细胞的作用。方法 应用免疫组化法检测MIR不同时期心肌FOS蛋白的表达,并采用末端标记技术对心肌细胞凋亡数进行检测。结果 ①对照组心肌无FOS蛋白表达,亦未见凋亡细胞出现。②与MIR组相比,TMP干预组心肌FOS蛋白的表达明显减弱(60 min分别为57±44个/片和6.4±3.2个/片,90 min分别为467±450个/片和171±160个/片,120 min分别为246±160个/片和130±121个/片,均P<0.05),TUNEL阳性细胞数均明显减少(60 min分别为36.3±8.7个/片和24.7±7.2个/片,P<0.05; 120 min分别为48.0±23.8个/片和10.0±8.1个/片, P<0.01)。结论 MIR可诱导终末分化的心肌细胞高表达FOS蛋白及发生细胞凋亡;应用TMP可使缺血心肌细胞c-fos基因表达减弱及凋亡减轻。
Abstract:
AIM To study the effects of tetramethylpyrazine (TMP) on c-fos expression and apoptosis of myocardial cells in myocardial ischemic reperfusion (MIR) in rats. METHODS Coloring TDT-mediated dutp nick end labeling (TUNEL) and immunohistochemical staining were used. RESULTS ①No blue apoptosis cells and FOS protein expression were found in non-ischemic myocardial tissues; ②Compared with those of MIR rats, the number of FOS immunoreactive positive cells in rats treated with TMP decreased significantly (from 57±44/section to 6.4±3.2/section, 467±450/section to 171±161/section and 246±160/section to 130±121/section respectively, P<0.05 ) in 60, 90 and 120 min and the number of TUNEL positive cells in rats treated with TMP also decreased significantly ( from 36.3±8.7/section to 24.7±7.2/section and 48.0±23.8/section to 10.0±8.1/section respectively, P<0.01) in 60 minutes and 120 minutes. CONCLUSION Myocardial cells may induce apoptosis in MIR and apoptosis may be related to the increased c-fos expression. Administration of TMP can decrease the expression of c-fos and the apoptosis of myocardial cells in MIR.

参考文献/References

[1] Gottlieb RA,Burlesen KO,Kloner RA,et al. Reperfusion injury induces apoptosis in rabit cardiomyocytes[J]. J Clin Invest, 1994,94(4):1621.

[2] 胡 萍,尤家禄,罗 正. 大鼠心脏再灌注损伤模型[J]. 湖南医学院学报, 1986,11(1):17.

[3] Das DK,Engelman RM. Molecular adaptation of cellular defences following preconditioning of the heart by repeated ischemia[J]. Cardiovas Res, 1993,27(4):578.

[4] Wihsman JH. A new method to detect apoptosis in paraffin sections:in situ end-labeling of fragmented DNA[J]. J Histochem Cytochem, 1993,41(1):7.

[5] 罗 义, 李卓仁, 郭南山. 心血管疾病中的细胞凋亡[J]. 中华内科杂志, 1998,37(3):207.

[6] 王玉良, 巴彦坤. 川芎嗪对心血管的药理和电生理作用—一种新的钙拮抗剂[J]. 中西医结合杂志, 1995,15(6):291.

[7] Kwan CY,Daniel EF. Inhibitor of vasoconstriction by tetramethyl pyrazine:Does it act by blocking votage dependent Ca channel[J]? Cardiovasc pharmacol, 1990,15(2):157.

[8] Morgan J, Curran T. Role of ion flux in the control of c-fos expression[J]. Nature, 1986,322(6079):552.

备注/Memo

备注/Memo:
收稿日期:1999-04-15.
更新日期/Last Update: 2000-05-25