温阳活血利尿可抑制胶原纤维和心肌纤维化,减轻线粒体信号通路介导的慢性心力衰竭大鼠心肌凋亡,从而减轻心肌损伤。

IF 1.7 4区 医学 Q2 MEDICINE, GENERAL & INTERNAL Tohoku Journal of Experimental Medicine Pub Date : 2024-07-11 Epub Date: 2024-03-22 DOI:10.1620/tjem.2024.J022
Yong Chen, Yadan Tu, Lei Du, Ruixue Nan, Yi Ren
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引用次数: 0

摘要

温阳活血利尿汤(WYPBD)已被证实能有效治疗某些疾病。本研究旨在评估温阳利水丸治疗慢性心力衰竭(CHF)的疗效。通过腹腔注射多柔比星(DOX)建立慢性心力衰竭大鼠。分析了 WYPBD 对心功能和心肌组织血流动力学参数的治疗效果。评估了胶原纤维的生成和心肌纤维化。用 RT-PCR 评估了 COL1A1 基因、COL3A1 基因和 TGFB1 基因的转录。评估心肌组织中 BNP、AVP、PARP、caspase-3 和 Bcl-2 的表达。用 TUNEL 法检测心肌细胞凋亡。与 CHF 模型组大鼠相比,WYPBD 可减轻 CHF 大鼠心肌肥厚的程度(P < 0.05)。与 CHF 模型组大鼠相比,WYPBD 可明显改善 CHF 大鼠的心脏血流动力学(增加 LVEF 和 LVSF)(P < 0.05)。WYPBD 可保护 CHF 大鼠心肌结构并抑制心肌组织中胶原纤维的生成。与 CHF 模型组相比,WYPBD 可显著降低 CHF 大鼠心肌组织中心肌纤维化介质(Col1α、Col3α、TGF-β1)的转录(P < 0.05)。与 CHF 模型组大鼠相比,WYPBD 可明显降低 CHF 大鼠心肌组织中 BNP 和 AVP 的表达(P < 0.05)。与 CHF 模型组大鼠相比,WYPBD 可明显降低 CHF 大鼠心肌组织中 PRAP 和 caspase-3 的表达,增加 Bcl-2 的表达(P < 0.05)。总之,WYPBD通过抑制胶原纤维和心肌纤维化,减轻与心肌细胞线粒体信号通路相关的细胞凋亡,从而减轻CHF心肌损伤。
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Warming Yang Promoting Blood Circulation and Diuresis Alleviates Myocardial Damage by Inhibiting Collagen Fiber and Myocardial Fibrosis and Attenuating Mitochondria Signaling Pathway Mediated Apoptosis in Chronic Heart Failure Rats.

Warming Yang promoting blood circulation and diuresis (WYPBD) has been proven effective in treating some diseases. This study aimed to evaluate therapeutic effect of WYPBD in treating chronic heart failure (CHF). CHF rats were established by intraperitoneally injecting doxorubicin (DOX). Therapeutic effects of WYPBD on cardiac function and hemodynamic parameters of myocardial tissues were analyzed. Collagen fiber production and myocardial fibrosis were evaluated. Transcriptions of COL1A1 gene, COL3A1 gene, and TGFB1 gene were evaluated with RT-PCR. Expression of BNP, AVP, PARP, caspase-3, and Bcl-2 in myocardial tissues were evaluated. TUNEL assay was used to identify apoptosis of cardiomyocytes. WYPBD alleviated degree of myocardial hypertrophy in CHF rats compared to the rats in CHF model group (P < 0.05). WYPBD significantly improved cardiac hemodynamics (increased LVEF and LVSF) of CHF rats compared to rats in the CHF model group (P < 0.05). WYPBD protected myocardial structure and inhibited collagen fiber production in myocardial tissues of CHF rats. WYPBD markedly decreased myocardial fibrosis mediators (Col1α, Col3α, TGF-β1) transcription in myocardial tissues of CHF rats compared to rats in CHF model group (P < 0.05). WYPBD significantly reduced BNP and AVP expression in myocardial tissues of CHF rats compared to rats in the CHF model group (P < 0.05). WYPBD markedly reduced the expression of PRAP and caspase-3, and increased Bcl-2 expression in myocardial tissues of CHF rats compared to rats in the CHF model group (P < 0.05). In conclusion, WYPBD alleviated CHF myocardial damage by inhibiting collagen fiber and myocardial fibrosis, attenuating apoptosis associated with the mitochondria signaling pathway of cardiomyocytes.

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