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非诺贝特对压力超负荷大鼠心肌细胞凋亡和凋亡相关基因Fas、FasL表达的影响(PDF)

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2007年第5期
页码:
511-504/509
栏目:
基础研究
出版日期:
2007-10-01

文章信息/Info

Title:
Effects of Fenofibrate on cardiomyocyte apoptosis and expression of apoptosisassociated gene Fas and FasL in pressure overload rats
作者:
吴强1; 杨永曜1 ; 李隆贵2 ; 杨天和1 ; 蔡运昌1 ; 蒋清安1
1. 贵州省人民医院心内科，贵州 贵阳 550002；2. 第三军医大学附属新桥医院心内科，重庆400037
Author(s):
WU Qiang1;  YANG Yongyao1;  LI Longgui2;  YANG Tianhe1;  CAI Yunchang1;  JIANG Qing an1
1.Department of Cardiology, Guizhou Province People′s Hospital, Guiyang 550002, Guizhou, China; 2.Department of Cardiology, Xinqiao Hospital, Third Military Medical University, Chongqing 400037, China
关键词:
过氧化物酶体增殖物活化型受体; 非诺贝特; 凋亡; 压力超负荷; 基因
Keywords:
peroxisome proliferatoractivated receptors;  fenofibrate;  apoptosis;  pressure overload;  gene
分类号:
R542.2
DOI:
-
文献标识码:
A
摘要:
目的 探讨过氧化物酶体增殖物激活型受体α(PPARα)配体非诺贝特对压力超负荷致大鼠左心室肥厚过程中心肌细胞凋亡的调控，并观察其对凋亡相关基因Fas/ FasL表达变化的影响。 方法 雄性Wistar大鼠腹主动脉缩窄致压力超负荷模型，术后48 h存活的大鼠随机分成：单纯模型组术后4周亚组、单纯模型组术后8周亚组、非诺贝特干预组术后4周亚组、非诺贝特干预组术后8周亚组。以假手术组为对照。分别于给药处理4周和8周后观察心室重构指标、心肌细胞凋亡指数（CAI）及凋亡相关基因Fas/FasL蛋白表达的变化。 结果 与同期单纯模型组比较，非诺贝特干预组术后4周亚组的心室重构指标、CAI及Fas/FasL表达差异无显著性，但非诺贝特干预8周可显著减轻压力超负荷诱导的心肌肥厚，降低CAI，下调Fas/FasL的表达。 结论 PPARα配体长期干预（8周）能减轻压力超负荷大鼠的心肌肥厚，抑制心肌细胞凋亡，对心力衰竭进程中的心室重构具有抑制作用；凋亡相关基因Fas和FasL参与了PPARα途径对心肌细胞凋亡的调控。
Abstract:
AIM To investigate the effects of ligands of PPARα fenofibrate on cardiomyocyte apoptosis and expression of apoptosisassociated gene, Fas and Fas ligand (FasL) in pressure overload rats. METHODS A pressure overloading model was established by abdominal aorta constriction in Wistar rats. Fortyeight hours after constriction, the surviving rats were randomly divided into 4 groups: 4week coarctation of abdominal aorta group, 8week coarctation of abdominal aorta group, 4week Fenofibrate ［30 mg/(kg·d)］ treatment group and 8week Fenofibrate treatment group. Additional 10 rats that underwent abdominal cavity incision without ligation served as sham group. After 4 weeks and 8 weeks of therapy, the ratio of left ventricular weight to body weight (LVW/BW) and the ratio of right ventricular weight to body weight (RVW/BW) were measured. DNA fragmentations were determined semiquantitatively by in situ TDTmediated dUTP nick end labeling (TUNEL). Using Western blot, Fas and FasL expression was detected. RESULTS Fenofibrate treatment for 8 week significantly reduced LVW/BW, cardiomyocyte apoptosis and expression of Fas and FasL in pressure overload rats. In contrast, there was no significant difference in the above mentioned indices between the group with aortic constriction and the group treated with 4week Fenofibrate. CONCLUSION Chronic treatment (8 weeks) with the PPARα agonist may be useful in preventing cardiac hypertrophy and apoptosis. The protooncogene Fas and FasL play a key role in PPARα pathway, regulating cardiocyte apoptosis.

参考文献/References

［1］ Strakova N, Ehrmann J, Bartos J, et al. Peroxisome proliferatoractivated receptors (PPAR) agonists affect cell viability, apoptosis and expression of cell cycle related proteins in cell lines of glial brain tumors［J］. Neoplasma, 2005, 52 (2): 126-136.

［2］ Muzio G, Martinasso G, Trombetta A, et al. HMG-CoA reductase and PPARalpha are involved in clofibrateinduced apoptosis in human keratinocytes［J］. Apoptosis, 2006, 11 (2): 265-275.

［3］ Kubota T, Yano T, Fujisaki K, et al. Fenofibrate induces apoptotic injury in cultured human hepatocytes by inhibiting phosphorylation of Akt［J］. Apoptosis, 2005, 10 (2): 349-358.

［4］ Wang H, Nawata J, Kakudo N, et al. The upregulation of ICAM1 and Pselectin requires high blood pressure but not circulating reninangiotensin system in vivo［J］. J Hypertens, 2004, 22 (7): 1323-1332.

［5］ Wencker D, Chandra M, Nguyen K, et al. A mechanistic role for cardiac myocyte apoptosis in heart failure［J］. J Clin Invest, 2003, 111 (10): 1497-1504.

［6］ 吴强, 李隆贵, 蔡运昌, 等. 心衰大鼠心肌核因子κB活化及其与心肌细胞凋亡的关系［J］. 中国病理生理杂志, 2003, 19 (5): 649-652.

［7］ Liang F, Wang F, Zhang S, et al. Peroxisome proliferator activated receptor (PPAR) alpha agonists inhibit hypertrophy of neonatal rat cardiac myocytes［J］. Endocrinology, 2003, 144(9): 4187-4194.

备注/Memo

备注/Memo:
收稿日期：2006-07-18.基金项目：贵州省优秀科技教育人才省长专项资金项目资助（黔科教办200304）；贵州省科技攻关项目资助（黔科合2004NGY043）通讯作者：吴强，博士，副主任医师，主要从事心血管病基础与临床研究Email：waqqaa@yahoo.com.cn
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