Qingda granule prevents Ang II-induced cardiac hypertrophy via inhibiting NF-κB signaling pathway.

IF 4.8 2区 医学 Q1 PHARMACOLOGY & PHARMACY
Frontiers in Pharmacology Pub Date : 2025-09-16 eCollection Date: 2025-01-01 DOI:10.3389/fphar.2025.1603316
Yuhang Gong, Da Wo, Canran Wang, Ruokun Huang, En Ma, Celiang Wu, Jun Peng, Weidong Zhu, Dan-Ni Ren
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引用次数: 0

Abstract

Background: Angiotensin II (Ang II) type 1 receptor (AT1R) signaling pathway is a key component of the renin-angiotensin-aldosterone system (RAAS) that is involved in the development of hypertension. Chronic Ang II overactivation results in pathological cardiac hypertrophy that progresses into decompensated cardiac dysfunction and impairment. Qingda granule (QDG) is a Traditional Chinese formula that has been used clinically in treating hypertension and its complications.

Purpose: This study aimed to elucidate the role and underlying mechanisms of QDG in preventing Ang II-induced cardiac hypertrophy.

Methods: We used chronic Ang II infusion via minipumps in mice and administered QDG daily to examine the effects of QDG on preventing hypertension and various parameters of cardiac impairment.

Results: QDG treatment significantly reduced Ang II-induced elevation in blood pressure. Furthermore, QDG exerted a robust cardioprotective effect on chronic Ang II-induced cardiac hypertrophy and decompensated cardiac dysfunction. QDG also inhibited Ang II-induced adverse NF-κB signaling activation and downstream pro-inflammatory targets, which were prevented via administration with SC75741, a specific NF-κB inhibitor.

Conclusion: Our findings provide further insight into the robust ability of QDG in preventing Ang II-induced cardiac hypertrophy via preventing NF-κB signaling activation and implicate its use in the clinical treatment of hypertension and cardiac hypertrophy.

清大颗粒通过抑制NF-κB信号通路抑制angii诱导的心肌肥厚。
背景:血管紧张素II (Ang II) 1型受体(AT1R)信号通路是肾素-血管紧张素-醛固酮系统(RAAS)的关键组成部分,参与高血压的发展。慢性Ang II过度激活导致病理性心脏肥大,并发展为失代偿性心功能障碍和损害。清大颗粒(QDG)是临床上用于治疗高血压及其并发症的中药方剂。目的:本研究旨在阐明QDG在预防angii诱导的心肌肥厚中的作用及其机制。方法:采用小鼠微泵慢性输注angii,每日给药QDG,观察QDG对高血压和心脏各参数损害的预防作用。结果:QDG治疗可显著降低Ang ii诱导的血压升高。此外,QDG对慢性angii诱导的心脏肥厚和失代偿性心功能障碍具有强大的心脏保护作用。QDG还抑制Ang ii诱导的不良NF-κB信号激活和下游促炎靶标,这些靶标可通过给药SC75741(一种特异性NF-κB抑制剂)来阻止。结论:我们的研究结果进一步揭示了QDG通过阻止NF-κB信号激活来预防Ang ii诱导的心脏肥厚的强大能力,并暗示其在高血压和心脏肥厚的临床治疗中的应用。
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来源期刊
Frontiers in Pharmacology
Frontiers in Pharmacology PHARMACOLOGY & PHARMACY-
CiteScore
7.80
自引率
8.90%
发文量
5163
审稿时长
14 weeks
期刊介绍: Frontiers in Pharmacology is a leading journal in its field, publishing rigorously peer-reviewed research across disciplines, including basic and clinical pharmacology, medicinal chemistry, pharmacy and toxicology. Field Chief Editor Heike Wulff at UC Davis is supported by an outstanding Editorial Board of international researchers. This multidisciplinary open-access journal is at the forefront of disseminating and communicating scientific knowledge and impactful discoveries to researchers, academics, clinicians and the public worldwide.
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