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Ling-Gui-Zhu-Gan Decoction Ameliorates Heart Failure via Modulating Energy Metabolism and Lipid Homeostasis: Insights from Transcriptomics and Lipidomics

ABSTRACT: Background: Heart failure (HF) remains a global health challenge with limited therapeutic options. Ling-Gui-Zhu-Gan Decoction (LGZGD), a traditional Chinese medicine formula, has shown clinical efficacy in HF treatment, yet its molecular mechanisms remain unclear. Methods: This study investigated LGZGD's cardioprotective effects and underlying mechanisms using a doxorubicin-induced HF mouse model. Mice were divided into blank (KB), model (M), trimetazidine (QM), and LGZGD (LG) groups. Cardiac function was assessed via echocardiography, while myocardial injury and fibrosis were evaluated through histopathology. Transcriptomics and lipidomics analyses were performed to identify molecular pathways. Results: LGZGD significantly improved ejection fraction (EF) and fractional shortening (FS), alleviated myocardial vacuolization, and reduced fibrosis, outperforming trimetazidine. Transcriptomics revealed LGZGD modulated oxidative phosphorylation and ATP synthase activity, restoring energy metabolism. Lipidomics highlighted its regulation of glycerophospholipid metabolism, particularly phosphatidylethanolamine (PE) and phosphatidylcholine (PC), linked to anti-inflammatory and lipid homeostasis effects. Conclusion: Integrated omics data suggested LGZGD ameliorates HF by enhancing mitochondrial function, mitigating oxidative stress, and balancing lipid metabolism. These findings provide mechanistic insights into LGZGD's therapeutic benefits, supporting its potential as a multi-targeted intervention for HF through energy and lipid metabolic regulation.

ORGANISM(S): Mus musculus

PROVIDER: GSE305559 | GEO | 2025/08/20

REPOSITORIES: GEO

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Project description:Impaired myocardial contractile function is a hallmark of heart failure (HF) which may present under resting conditions and/or during physiological stress. Previous studies reported that high fat feeding in HF is associated with improved myocardial contractile function at baseline. Our goal was to determine whether myocardial function is compromised in response to physiological stress and to evaluate the global gene expression profile of rats fed high dietary fat following infarction. Male Wistar rats underwent ligation or sham surgery and were fed normal (10% kcal fat) (SHAM+NC, HF+NC) or high fat (60% kcal saturated fat) (SHAM+SAT, HF+SAT) for 8 weeks. Myocardial contractile function was assessed using a Millar pressure-volume (PV) conductance catheter at baseline, during inferior vena caval occlusions and dobutamine (DOB) stress. Steady state indices of systolic function, left ventricular (LV)+dP/dtmax, stroke work and maximal power were increased in HF+SAT vs HF+NC; HF+NC were reduced vs SHAM+NC. Preload-recruitable measures of contractility [end systolic PV relationship, maximal elastance, preload recruitable SW and peak+dP/dtmax to end diastolic volume] were decreased in HF+NC but not HF+SAT. β-adrenergic responsiveness (delta-LV+dP/dtmax and delta-cardiac output DOB 0-10 µg•kg-1•min-1) was reduced in HF, but high fat feeding did not further impact contractile reserve in HF. Contractile reserve was reduced by high fat in SHAM+SAT. Microarray gene expression analysis reveals the majority of significantly altered pathways identified to contain multiple gene targets correspond to cell signaling pathways and energy metabolism. These findings suggest that high saturated fat improves myocardial function at rest and during physiological stress in infarcted hearts, but may negatively impact contractile reserve under non-pathological conditions. Furthermore, high fat feeding-induced alterations in gene expression related to energy metabolism and specific signaling pathways reveal promising targets through which high saturated fat potentially mediates cardioprotection in heart failure/LV dysfunction.

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Ling-Gui-Zhu-Gan Decoction Ameliorates Heart Failure via Modulating Energy Metabolism and Lipid Homeostasis: Insights from Transcriptomics and Lipidomics

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