足部休克应激下大鼠心脏细胞凋亡状况

Regina Célia Spadari-Bratfisch, Viviane de Menezes Cáceres, Daniela Ortolani, Viviane Carlin, Daniel Araki Ribeiro
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引用次数: 2

摘要

背景与目的:本研究的目的是探讨物理应激是否能够调节大鼠心肌组织的凋亡反应。观察足部休克应激对p53、bcl-2和bax的组织病理学变化和免疫组化的影响。方法:雄性Wistar大鼠10只,随机分为对照组1组和应激组2组。压力方案包括连续三天每天进行一次足部电击。结果:各组心肌组织无明显变化。此外,足部休克应激不能调节p53、bcl-2或bax的表达,没有显著的统计学差异(P >各组间各免疫指标差异0.05)。结论:综上所述,我们的结果表明足部休克应激不会引起大鼠心肌组织的组织病理学改变。生理应激似乎不能调节大鼠的细胞凋亡反应。当然,这一发现为研究应激后细胞凋亡与心脏损伤之间的关系机制提供了新的见解。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Apoptosis status from rat heart submitted to foot shock stress

Background and aim: The goal of this study was to investigate whether physical stress is able to modulate apoptotic response in rat myocardial tissue. The effects of foot shock stress on the histopatological changes and immunohistochemistry for p53, bcl-2 and bax were evaluated. Methods: Male Wistar rats (n= 10) were distributed into two groups: group 1, control and group 2, stress. The stress protocol consisted of one daily foot-shock session applied on three consecutive days. Results: The results pointed out no remarkable changes of myocardial tissue between groups. Also, the foot shock stress was not able to modulate p53, bcl-2 or bax expression, as depicted by no significant statistically differences (P > 0.05) between groups for all immunomarkers evaluated. Conclusions: Taken together, our results suggest that foot shock stress did not induce histopathological changes in rat myocardial tissue. It seems that physical stress is not able to modulate apoptotic response in rats. Certainly, this finding offers new insights into the mechanisms underlying the relation between apoptosis and cardiac injury after stress.

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