Inflammatory markers in dependence on the plasma concentration of 37 fatty acids after the coronary stent implantation

Handl, Jiří; Meloun, Milan; Mužáková, Vladimíra

doi:10.1016/j.jpba.2017.10.033

Cited by 4 publications

(1 citation statement)

References 27 publications

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“…Previous study Chiva-Blanch et al (2016) demonstrated a higher percentage of serum oleic acid in acute myocardial infarction patients, and the elevated plasma oleic acid may cause endothelial dysfunction and atherosclerosis through sequential activation of protein kinase C (PKC) and NF-κB-dependent signaling pathways, which showed a highly correlation with inflammation ( Park et al, 2003 ). Moreover, palmitic acid, a 16-carbon saturated fatty acid, could induce apoptosis in endothelial cells via p38 and JNK mitogen-activated protein kinase pathways ( Jiang et al, 2010 ), and it can activate NF-κB-dependent signaling pathways to stimulate inflammatory responses ( Handl et al, 2018 ). Palmitic acid may also serve as a source of ROS through mitochondrial oxidation ( Stentz and Kitabchi, 2006 ).…”

Section: Discussionmentioning

confidence: 99%

Integration of Metabolomics With Pharmacodynamics to Elucidate the Anti-myocardial Ischemia Effects of Combination of Notoginseng Total Saponins and Safflower Total Flavonoids

Yuan

et al. 2018

Front. Pharmacol.

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Notoginseng (Sanqi), the roots and rhizomes of Panax notoginseng and safflower, the flowers of Carthamus tinctorius, are widely used traditional Chinese medicines (TCMs) for the treatment of cardiovascular diseases. Positive evidences have fueled growing acceptance for cardioprotective effects of the combination of the notoginseng total saponins and safflower total flavonoids (CNS) against myocardial ischemia (MI). However, the underlying cardioprotective mechanisms of CNS are still obscured. Metabolomics is a comprehensive tool for investigating biological mechanisms of disease, monitoring therapeutic outcomes, and advancing drug discovery and development. Herein, we investigated the cardioprotective effects of CNS on the isoproterenol (ISO)-induced MI rats by using plasma and urine metabolomics based on ultra-performance liquid chromatography coupled with quadrupole-time of flight mass spectrometry (UPLC-Q-TOF/MS) and multiple pharmacodynamics approaches. The results showed that pretreatment with CNS could attenuate the cardiac injury resulting from ISO, as evidenced by decreasing the myocardial infarct size, converting the echocardiographic, histopathological, and plasma biochemical abnormalities, and reversing the perturbations of plasma and urine metabolic profiles, particularly for the 55.0 mg/kg dosage group. In addition, 44 metabolites were identified as the potential MI biomarkers, mainly including a range of free fatty acids (FFAs), sphingolipids, and glycerophospholipids. CNS pretreatment group may robustly ameliorate these potential MI-related biomarkers. The accumulation of LysoPCs and FFAs, caused by PLA2, may activate NF-κB pathway and increase proinflammatory cytokines. However, our results showed that CNS at 55.0 mg/kg dosage could maximally attenuate the NF-κB signaling pathway, depress the expressions of TNF-α, IL-6, IL-1β, and PLA2. The results suggested that the anti-inflammatory property of CNS may contribute to its cardioprotection against MI. Our results demonstrate that the integrating of metabolomics with pharmacodynamics provides a reasonable approach for understanding the therapeutic effects of TCMs and CNS provide a potential candidate for prevention and treatment of MI.

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