Shen Qi Li Xin formula improves chronic heart failure through balancing mitochondrial fission and fusion via upregulation of PGC-1α.

IF 4.6 Q2 MATERIALS SCIENCE, BIOMATERIALS

ACS Applied Bio Materials Pub Date : 2021-10-18 DOI:10.1186/s12576-021-00816-y

Yan-Bo Sui, Jian Xiu, Jin-Xuan Wei, Pei-Pei Pan, Bi-Hong Sun, Li Liu

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引用次数: 4

Abstract

Background: Our previous study proved that Shen Qi Li Xin formula (SQLXF) improved the heart function of chronic heart failure (CHF) patients, while the action mechanism remains unclear.

Methods: H&E staining and TUNEL staining were performed to measure myocardial damages. Western blot was used to examine the expression of proteins. Moreover, CCK-8 assay and flow cytometry were used to measure cell viability and cell apoptosis, respectively. Concentrations of ATP and ROS in cells, and mitochondrial membrane potential (MMP) were detected to estimate oxidative stress.

Results: In vivo, we found that SQLXF improved cardiac hemodynamic parameters, reduced LDH, CK-MB and BNP production, and attenuated myocardial damages in CHF rats. Besides, SQLXF promoted mitochondrial fusion-related proteins expression and inhibited fission-related proteins expression in CHF rats and oxygen glucose deprivation/reoxygenation (OGD/R)-induced cardiac myocytes (CMs). In vitro, our data show that certain dose of SQLXF inhibited OGD/R-induced CMs apoptosis, cell viability decreasing and oxidative stress.

Conclusion: Overall, certain dose of SQLXF could effectively improve the cardiac function of CHF rats through inhibition of CMs apoptosis via balancing mitochondrial fission and fusion. Our data proved a novel action mechanism of SQLXF in CHF improvement, and provided a reference for clinical.

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神气理心方通过上调 PGC-1α 来平衡线粒体的分裂和融合，从而改善慢性心力衰竭。

背景：方法：H&E 染色和 TUNEL 染色测量心肌损伤。方法：采用 H&E 染色和 TUNEL 染色法检测心肌损伤情况，采用 Western 印迹法检测蛋白质表达情况。此外，CCK-8 检测法和流式细胞术分别用于测量细胞活力和细胞凋亡。检测细胞中 ATP 和 ROS 的浓度以及线粒体膜电位（MMP），以评估氧化应激：结果：在体内，我们发现 SQLXF 可改善 CHF 大鼠的心脏血流动力学参数，降低 LDH、CK-MB 和 BNP 的产生，减轻心肌损伤。此外，SQLXF 还能促进线粒体融合相关蛋白的表达，抑制线粒体裂变相关蛋白在 CHF 大鼠和氧糖剥夺/复氧（OGD/R）诱导的心肌细胞（CMs）中的表达。在体外，我们的数据显示一定剂量的 SQLXF 可抑制 OGD/R 诱导的 CMs 细胞凋亡、细胞活力下降和氧化应激：总之，一定剂量的SQLXF可通过平衡线粒体的裂变和融合，抑制CMs凋亡，从而有效改善CHF大鼠的心功能。我们的数据证明了 SQLXF 在改善 CHF 方面的新作用机制，并为临床提供了参考。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

ACS Applied Bio Materials Chemistry-Chemistry (all)

CiteScore

9.40

自引率

2.10%

发文量

464