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心脏收缩力调制对慢性心力衰竭家兔心肌细胞自噬和凋亡的影响。

Effects of cardiac contractility modulation on autophagy and apoptosis of cardiac myocytes in rabbits with chronic heart failure.

作者信息

Hao Qingqing, Lv Shilin, Zhang Jing, Liu Huiliang

机构信息

Hebei General Hospital, Shijiazhuang City, Hebei Province, P.R. China.

Hebei Medical University, Shijiazhuang City, Hebei Province, P.R. China.

出版信息

PLoS One. 2024 Dec 19;19(12):e0306242. doi: 10.1371/journal.pone.0306242. eCollection 2024.

DOI:10.1371/journal.pone.0306242
PMID:39700201
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11658494/
Abstract

BACKGROUND

Cardiac contractility modulation (CCM) is non-excitatory electrical stimulation for improving cardiac function. This study aimed to evaluate the effects of CCM on autophagy and apoptosis of cardiac myocytes in a rabbit model of chronic heart failure (CHF) and explore its possible mechanism.

METHODS

Thirty rabbits were randomised into the Sham, heart failure (HF) and CCM groups, and animals in all three groups were sacrificed after 16 weeks of ascending aortic constriction or sham surgery. The expression of autophagy associated protein LC3 was observed by immunofluorescence staining. With Western-blot measured the expression of Beclin1, P62, LC3B (II/I) and Bcl-2, ALDH2, Bax and Caspase-3 protein in myocardial tissue. The apoptosis rate and the apoptosis of myocardial cells was observed by flow cytometry and TUNEL method.

RESULTS

  1. In comparison to the Sham group, the expression of LC3 and Beclin1 was significantly increased, and the expression of p62 protein was decreased in the heart tissues of rabbits in the HF group. Compared with HF group, after CCM intervention, the expression of Beclin1 and LC3B proteins decreased, while the P62 protein increased, and the LC3B(II/I) ratio decreased (P<0.05). 2) The expression of Bcl-2, ALDH2 protein and Bcl-2 mRNA decreased compared with the Sham group (P<0.05), while the expression of Bax, Caspase-3 protein and mRNA was significantly increased (P<0.05). However, the expression of ALDH2 mRNA in the CCM group was not statistically significant. The expression of Bcl-2, ALDH2 protein and mRNA increased after CCM intervention, and the expression of Bax, Caspase-3 protein and mRNA decreased (P<0.05). 3) The apoptosis situation in the Sham group was similar to that of normal myocardium, compared with the Sham group, the number of apoptotic bodies increased, and the apoptosis percentage of cardiomyocytes increased significantly (P<0.05). After CCM intervention, the number of apoptotic bodies and the percentage of apoptosis decreased compared with the HF group (P<0.05).

CONCLUSIONS

The intervention of CCM has been shown to enhance both myocardial systolic and diastolic function in rabbits with CHF. The mechanism may be related to the inhibition of cardiomyocyte autophagy by regulating the expression levels of Beclin1, P62, and LC3B(II/I) in cardiomyocytes, as well as the reversal of cardiomyocyte apoptosis by regulating the expression levels of Bcl-2, ALDH2, Bax, and Caspase-3 in cardiomyocytes.

摘要

背景

心脏收缩力调制（CCM）是一种用于改善心脏功能的非兴奋性电刺激。本研究旨在评估CCM对慢性心力衰竭（CHF）兔模型中心肌细胞自噬和凋亡的影响，并探讨其可能机制。

方法

将30只兔子随机分为假手术组、心力衰竭（HF）组和CCM组，三组动物在进行升主动脉缩窄或假手术后16周处死。通过免疫荧光染色观察自噬相关蛋白LC3的表达。采用蛋白质免疫印迹法检测心肌组织中Beclin1、P62、LC3B（II/I）以及Bcl-2、ALDH2、Bax和Caspase-3蛋白的表达。通过流式细胞术和TUNEL法观察心肌细胞的凋亡率及凋亡情况。

结果

1）与假手术组相比，HF组兔心脏组织中LC3和Beclin1的表达显著增加，p62蛋白表达降低。与HF组相比，CCM干预后，Beclin1和LC3B蛋白表达降低，而P62蛋白增加，且LC3B（II/I）比值降低（P<0.05）。2）与假手术组相比，Bcl-2、ALDH2蛋白及Bcl-2 mRNA表达降低（P<0.05），而Bax、Caspase-3蛋白及mRNA表达显著增加（P<0.05）。然而，CCM组中ALDH2 mRNA的表达无统计学意义。CCM干预后，Bcl-2、ALDH2蛋白及mRNA表达增加，Bax、Caspase-3蛋白及mRNA表达降低（P<0.05）。3）假手术组的凋亡情况与正常心肌相似，与假手术组相比，HF组凋亡小体数量增加，心肌细胞凋亡百分比显著升高（P<0.05）。CCM干预后，与HF组相比，凋亡小体数量及凋亡百分比降低（P<0.05）。

结论

已证明CCM干预可增强CHF兔的心肌收缩和舒张功能。其机制可能与通过调节心肌细胞中Beclin1、P62和LC3B（II/I）的表达水平抑制心肌细胞自噬，以及通过调节心肌细胞中Bcl-2、ALDH2、Bax和Caspase-3的表达水平逆转心肌细胞凋亡有关。

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