SurveyStress activated cytokines and the heart
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Cited by (91)
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2024, Environmental ResearchLong-term oral Asperosaponin VI attenuates cardiac dysfunction, myocardial fibrosis in a rat model of chronic myocardial infarction
2012, Food and Chemical ToxicologyCitation Excerpt :These data indicated that increasing in myocardial antioxidant enzymes and reducing IS contributed to sustaining cardiac function subsequent to MI, and these might be an important pathway in the cardioprotection of ASA VI in rat model of chronic MI. Oxidative stress is a powerful stimulant for the increased expression of pro-inflammatory cytokines (Mak and Newton, 2001), which of themselves can result in further myocardial depression, direct cytotoxicity and further oxidative stress (Mann, 1996). In this study, treatment with ASA VI significantly decreased the levels of TNF-α and IL-6 in MI rats.
The Cardiovascular System
2012, The Laboratory MouseProtective effects of vanillic acid on electrocardiogram, lipid peroxidation, antioxidants, proinflammatory markers and histopathology in isoproterenol induced cardiotoxic rats
2011, European Journal of PharmacologyCitation Excerpt :The observed increase in the expression of these pro-inflammatory cytokine genes might be due to oxidative stress in isoproterenol induced cardiotoxic rats. In this context, previous studies have shown that oxidative stress is a powerful stimulant for the pro-inflammatory cytokines (Mak and Newton, 2001) which of themselves can result in further myocardial depression, adverse ventricular remodeling, direct cytotoxicity and further oxidative stress (Mann, 1996). Vanillic acid pretreatment decreased the expression of these pro-inflammatory cytokine genes in the myocardium of isoproterenol induced cardiotoxic rats.
Changes in natriuretic peptide and cytokine plasma levels in patients with heart failure, after treatment with high dose of furosemide plus hypertonic saline solution (HSS) and after a saline loading
2011, Nutrition, Metabolism and Cardiovascular DiseasesCitation Excerpt :Hemodynamic pressure overloading provoked a robust, albeit transient, increase in proinflammatory cytokine and cytokine receptor gene expression in the adult mammalian heart. This observation suggested the possibility that proinflammatory cytokine expression is modulated through load-dependent mechanisms [23]. This issue also appears confirmed by our study that reported how volume depletion due to high dosage furosemide is able to induce a significant lowering of cytokine plasma levels only partially restored by acute volume loading.