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腺嘌呤核甘酸转运子-1在大鼠压力超负荷致心肌重塑中的表达

The expression of adenine nucleotide translocator-1 on pressure overload induced heart remodeling in rats
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摘要 目的:探讨心肌线粒体腺嘌呤核甘酸转运子-1(adeninenucleotidetranslocator-1,ANT1)对压力超负荷致心肌重塑的影响。方法:利用腹主动脉缩窄法建立大鼠压力超负荷模型,假手术组大鼠3只作为对照组。观察时间点为术后1,2,4,7,14,21和30天。ANT1mRNA含量的测定采用RT-PCR法,利用TUNEL法检测心肌细胞的凋亡。心肌纤维化的改变采用心肌胶原形态定量分析。结果:①与对照组比较,缩窄后4天ANT1mRNA的含量上调,并于第7天达到峰值,术后14天其含量回落至对照组水平,并保持至30天。②手术组心肌细胞凋亡在术后1天即升高,在4天时进入高峰期并持续至7天,其后低水平持续存在,直至实验结束。而对照组未发现凋亡的存在。③与对照组比较,心肌胶原容积分数于术后14天方明显增加,并持续增高。结论:ANT1参与了压力超负荷致心肌重塑早期心肌细胞凋亡的调节,并可能影响了这一过程的发生和发展。 Objective:To explore the effects of adenine nucleotide translocator-1 (ANT1) on pressure overload induced heart remodeling.Method:The pressure overload animal model was established in rats by abdomial aorta coarctation, and 3 sham-operated rats served as control. The time course was 1, 2, 4, 7, 14, 21, and 30 days after operation. The mRNA expression of ANTI was evaluated by RT-PCR. The TUNEL method was applied to detect the myocardial apoptosis. The myocardial fibrosis was characterized by cardiac collagen morphological quantitive analyses.Result:①Compared with the control group, the expression of ANTI mRNA was upregulated on the 4th day after coarctation, and peaked in clays seventh, and then it returned to control level in day 14th and persisted for 30 days. ②The apoptosis increased significantly on the first day, and reached a plateau between 4th and 7th day, afterwards, it decreased continuously to low level. However, the apoptosis was so rare that it was undetectable in the control group. ③Compared with control group, the cardiac collagen volume fraction(CVF) did not increased until day 14th and developed continuously afterward. Conclusion:The ANTI participates in the regulation of apoptosis during the early stage of pressure overload induced heart remodeling, and may influence the development of the process.
出处 《中国康复医学杂志》 CAS CSCD 北大核心 2005年第12期897-901,共5页 Chinese Journal of Rehabilitation Medicine
关键词 腺嘌呤核苷酸转运子-1 凋亡 心肌重塑 压力超负荷 大鼠 adenine nucleotide translocator-1 apoptosis heart remodeling pressure overload rat
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