Qiliqiangxin capsule alleviates cardiac hypertrophy and cardiac dysfunction by regulating miR-382-5p/ATF3 axis.

IF 2.2 4区医学 Q2 MEDICINE, GENERAL & INTERNAL Clinics Pub Date : 2024-09-26 DOI:10.1016/j.clinsp.2024.100496

Bao Yin, XiaoTong Jiang, XinFeng Chang, ChunHua Song

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Abstract

Objective: Qiliqiangxin Capsule (QL) was investigated for its possible role in cardiac hypertrophy in this study.

Methods: QL (0.5 mg/mL) was pre-treated in Neonatal Mouse Ventricular Cardiomyocytes (NMVCs) before induction of cardiomyocyte hypertrophy by Angiotensin II (Ang-II). Immunofluorescence staining for α-actinin was conducted to determine cell surface area. Atrial Natriuretic Peptide (ANP) and Brain Natriuretic Peptide (BNP) of hypertrophy markers were examined. Ang-II infusion was given to stimulate cardiac hypertrophy in mice. The cardiac function of mice was detected by echocardiography, and the pathological status of myocardial tissue was observed.

Results: The surface of cardiomyocytes was enlarged by Ang-II, and ANP and BNP levels were increased. QL processing could save these changes. miR-382-5p was upregulated in Ang-II-treated NMVCs, and reducing miR-382-5p could further enhance the therapeutic effect of QL while elevating miR-382-5p weakened the protective effect of QL. QL could inhibit miR-382-5p expression to negatively regulate Activated Transcription Factor 3 (ATF3) expression. Enhancing ATF3 expression rescued miR-382-5p upregulation-mediated role in NMVCs. In addition, QL alleviated Ang-II-stimulated cardiac hypertrophy and cardiac dysfunction in mice.

Conclusion: QL may alleviate cardiac hypertrophy and cardiac dysfunction via the miR-382-5p/ATF3 axis.

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芪蛭降糖胶囊通过调节miR-382-5p/ATF3轴缓解心肌肥厚和心功能不全

目的本研究探讨了芪蛭降糖胶囊（QL）在心肌肥大中可能发挥的作用：方法：在血管紧张素Ⅱ（Ang-Ⅱ）诱导心肌细胞肥大之前，将QL（0.5 mg/mL）预处理于新生小鼠室壁心肌细胞（NMVCs）中。对α-肌动蛋白进行免疫荧光染色以确定细胞表面积。还检测了肥大标志物心房钠尿肽（ANP）和脑钠尿肽（BNP）。输注 Ang-II 以刺激小鼠心脏肥大。通过超声心动图检测小鼠的心脏功能，并观察心肌组织的病理状态：结果：Ang-II 使心肌细胞表面增大，ANP 和 BNP 水平升高。miR-382-5p在Ang-II处理的NMVC中上调，降低miR-382-5p可进一步增强QL的治疗作用，而升高miR-382-5p则削弱QL的保护作用。QL 可抑制 miR-382-5p 的表达，从而负向调节活化转录因子 3（ATF3）的表达。增强 ATF3 的表达可挽救 miR-382-5p 在非小细胞肺癌中的上调作用。此外，QL 还能缓解 Ang-II 刺激的小鼠心肌肥厚和心功能不全：结论：QL可通过miR-382-5p/ATF3轴缓解心肌肥厚和心功能不全。

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

Clinics 医学-医学：内科

CiteScore

4.10

自引率

3.70%

发文量

129

审稿时长

52 days

期刊介绍： CLINICS is an electronic journal that publishes peer-reviewed articles in continuous flow, of interest to clinicians and researchers in the medical sciences. CLINICS complies with the policies of funding agencies which request or require deposition of the published articles that they fund into publicly available databases. CLINICS supports the position of the International Committee of Medical Journal Editors (ICMJE) on trial registration.