Exploring Potential Biomarkers of Blood Stasis Syndrome in Coronary Heart Disease and Association Between Platelet Metabolic Disorder and Myocardial Injury Based on Platelet Metabolomics
10.13422/j.cnki.syfjx.20260661
- VernacularTitle:基于血小板代谢组学探讨冠心病血瘀证的潜在生物标志物及血小板代谢紊乱与心肌损伤的关联
- Author:
Yanzhen ZHAO
1
;
Siyang BAI
1
;
Weixiong JIAN
1
;
Manli ZHOU
1
Author Information
1. Hunan Provincial Key Laboratory of Traditional Chinese Medicine Diagnostics，College of Chinese Medicine，Hunan University of Chinese Medicine，Changsha 410208，China
- Publication Type:Journal Article
- Keywords:
coronary heart disease;
blood stasis syndrome;
platelets;
metabolomics;
biomarker;
myocardial injury
- From:
Chinese Journal of Experimental Traditional Medical Formulae
2026;32(17):239-247
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveTo investigate the platelet metabolomic characteristics of the rat model of coronary heart disease （CHD） with blood stasis syndrome （BSS） based on ultra-high performance liquid chromatography coupled with quadrupole-Orbitrap high-resolution mass spectrometry （UPLC-Q-Exactive Orbitrap-MS）， screen potential biomarkers and metabolic pathway information， and elucidate the association mechanism between platelet metabolic disorders and myocardial injury. MethodsA total of 12 rats were randomized into a normal group and a modle group. The rat model of CHD-BSS was established by continuous high-fat feeding， intragastric administration of vitamin D3 in divided doses combined with subcutaneous injection of isoproterenol. Additionally， changes in standard lead Ⅱ electrocardiogram （ECG） and myocardial histopathological alterations of rats in the two groups were observed to evaluate myocardial injury in the modle group. After preprocessing of the untargeted metabolomic data of platelet samples from the two groups， multivariate statistical analysis and differential screening were performed sequentially. Principal component analysis （PCA） was performed to verify the separation of metabolic profiles of samples between groups. An orthogonal partial least squares-discriminant analysis （OPLS-DA） model was then constructed to preliminarily screen potential differential metabolites based on model parameters. Secondary screening was conducted with the fold change of metabolite expression to finally identify metabolites with significant intergroup differences， and metabolic pathway enrichment analysis was carried out based on these differential metabolites. Finally， potential platelet-specific biomarkers were identified based on receiver operating characteristic（ROC） curves. ResultsCompared with the normal group， the modle group presented obvious elevation of the J point and an ST-segment elevation greater than 0.1 mV on ECG， as well as pathological injuries such as loose arrangement of fibers and cellular vacuolar degeneration in the myocardial tissue. A total of 370 differentially expressed metabolites were dysregulated in the modle group， involving 8 significantly enriched metabolic pathways，such as purine metabolism， arachidonic acid metabolism， oxidative phosphorylation and adenosine monophosphate-activated protein kinase （AMPK） signaling pathway. Nine differential metabolites enriched in these pathways showed statistically significant differences in content. ROC curve analysis revealed that the area under the curve（AUC） of all characteristic metabolites was higher than 0.8. Among them， the AUC values of four metabolites， including sphinganine 1-phosphate， sphingosine 1-phosphate， 12-ketoleukotriene B4 and 14，15-dihydroxyeicosatrienoic acid， reached 1.0， indicating their potential as biomarkers. ConclusionPlatelet metabolic characteristics are significantly altered in the rat model of CHD-BSS. The screened potential biomarkers possess favorable diagnostic performance. The pathological changes mediated by these metabolites， including inflammatory response， thrombosis， and energy metabolism disorders， serve as critical mechanisms for abnormal platelet activation and subsequent myocardial injury. Platelet metabolomics provides a new perspective for the screening of biomarkers and research on pathological mechanisms of CHD-BSS.
