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tanshinone/infarkt
Veza se sprema u međuspremnik
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Tanshinone II A attenuates inflammatory responses of rats with myocardial infarction by reducing MCP-1 expression.
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The root of Salvia miltiorrhiza Bunge, a well-known traditional Chinese medicine, has been used effectively for the treatment of cardiovascular diseases for a long time. The mechanisms underlying this therapeutic effect are not, however, fully understood. Tanshinone IIA (Tan IIA) is one of the major
[Relationship between inhibitory action of tanshinone on neutrophil function and its prophylactic effects on myocardial infarction].
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In isoprenaline-induced myocardial infarction in rabbits, the circulating neutrophils (neu) were in an activated state. tanshinone (tan, ig) suppressed the neu functions (acid-phosphatase release, adhesiveness, and phagocytosis) dose-dependently and reduced myocardial necrosis concomitantly. There
Rationale and Design of Sodium Tanshinone IIA Sulfonate in Left Ventricular Remodeling Secondary to Acute Myocardial Infarction (STAMP-REMODELING) Trial: A Randomized Controlled Study.
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BACKGROUND
Left ventricular (LV) remodeling in ischemic cardiomyopathy is the leading cause of heart failure and is an established prognostic factor for adverse cardiovascular events. Experimental studies suggest that sodium tanshinone IIA sulfonate attenuates cardiac remodeling in animal models of
Tanshinone IIA increases recruitment of bone marrow mesenchymal stem cells to infarct region via up-regulating stromal cell-derived factor-1/CXC chemokine receptor 4 axis in a myocardial ischemia model.
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Systemic administration with bone marrow mesenchymal stem cells (BMSCs) is a promising approach to cure myocardial ischemia (MI), while the efficacy of cell transplantation is limited by the low engraftment of BMSCs. Tanshinone IIA (Tan IIA) has been reported many times for the treatment of MI.
Differential cardioprotective effects of salvianolic acid and tanshinone on acute myocardial infarction are mediated by unique signaling pathways.
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BACKGROUND
Salvianolic acid (SAL) and tanshinone (TAN) are major hydrophilic and lipophilic compounds, respectively, from one herbal medicine, Danshen, which has been widely and successfully used for treating cardiovascular diseases in Asian countries. Because few studies have reported different
Exploration of Multiple Signaling Pathways Through Which Sodium Tanshinone IIA Sulfonate Attenuates Pathologic Remodeling Experimental Infarction.
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The level of maladaptive myocardial remodeling consistently contributes to the poor prognosis of patients following a myocardial infarction (MI). In this study, we investigated whether and how sodium tanshinone IIA sulfonate (STS) would attenuate the post-infarct cardiac remodeling in mice model of
Tanshinone IIA prevents left ventricular remodelling via the TLR4/MyD88/NF-κB signalling pathway in rats with myocardial infarction.
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In this study, we aim to investigate the role of tanshinone IIA in myocardial infarction (MI), especially in left ventricular remodelling (VR) and the underlying mechanism involving the TLR4/MyD88/NF-κB signalling pathway. Sprague-Dawley (SD) rats (n = 96) were selected, and 12 of them underwent
Therapy for myocardial infarction: In vitro and in vivo evaluation of puerarin-prodrug and tanshinone co-loaded lipid nanoparticulate system.
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Myocardial infarction (MI) is the leading cause of morbidity and mortality worldwide. Nanoparticle systems carrying drugs have already been developed to treat MI. To improve the efficiency of tanshinone (TAN), and to achieve the synergistic effect of TAN and puerarin (PUE), PUE-prodrug and TAN
Protective effect of Tanshinone IIA against infarct size and increased HMGB1, NFκB, GFAP and apoptosis consequent to transient middle cerebral artery occlusion.
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Acute inflammation plays an important role in brain damage following cerebral ischemia and reperfusion (I/R) injury. The present study employed a rat model of middle cerebral artery occlusion to explore the neuroprotective effects of tanshinone IIA (TSN), which is widely used in China for treating
Tanshinone IIA inhibits miR-1 expression through p38 MAPK signal pathway in post-infarction rat cardiomyocytes.
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Tanshinone IIA is a fat-soluble pharmacologically active ingredient of Danshen, a well-known traditional Chinese medicine used for cardiovascular diseases such as coronary heart disease. Tanshinone IIA has been confirmed to suppress miR-1 and reduce the arrhythmogenesis after myocardial infarction
Regulation of antioxidant system, lipids and fatty acid β-oxidation contributes to the cardioprotective effect of sodium tanshinone IIA sulphonate in isoproterenol-induced myocardial infarction in rats.
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OBJECTIVE
Myocardial infarction (MI) is a cause of high morbidity and mortality in the world. Sodium tanshinone IIA sulphonate (STS) has been well used in Oriental medicine for treating cardiovascular diseases, however, the underlying mechanisms remain unclear. Alterations of circulating lipid
Protective effects of sodium tanshinone IIA sulfonate on cardiac function after myocardial infarction in mice.
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Sodium tanshinone IIA sulfonate (STS), a water-soluble derivative of tanshinone IIA, has been used in traditional Chinese medicine for many years. Many experiments have demonstrated that STS has anti-inflammatory, anti-apoptosis and angiogenesis effects. However, it is unclear whether STS has the
Nanoparticle-mediated delivery of Tanshinone IIA reduces adverse cardiac remodeling following myocardial infarctions in a mice model: role of NF-κB pathway.
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Our previous works have shown that tanshinone IIA inhibited maladaptive extracellular matrix remodeling in cardiac fibroblasts implicating its potential role in treating of pathologic cardiac remodeling. However, the intrinsically poor solubility and bioavailability of tanshinone IIA hindered its
Tanshinone inhibits neuronal cell apoptosis and inflammatory response in cerebral infarction rat model.
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We aimed to investigate the effect and mechanisms of tanshinone (TSN) IIA in cerebral infarction. The cerebral infarction rat model was established by middle cerebral artery occlusion (MCAO). After pretreatment with TSN, cerebral infarct volume, cerebral edema, and neurological deficits score were
Triphenylphosphonium and D-α-tocopheryl polyethylene glycol 1000 succinate-modified, tanshinone IIA-loaded lipid-polymeric nanocarriers for the targeted therapy of myocardial infarction.
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UNASSIGNED
Cardiovascular diseases (CVDs) are the leading causes of mortality worldwide. Currently, the best treatment options for myocardial infarction focus on the restoration of blood flow as soon as possible, which include reperfusion therapy, percutaneous coronary intervention, and therapeutic
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