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Tilianin pretreatment prevents myocardial ischemia-reperfusion injury via preservation of mitochondrial function in rat heart.
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BACKGROUND
Tilianin has been demonstrated to exert protective effects on the heart against ischemia-reperfusion (I/R) injury, yet whether it is beneficial to the mitochondria during myocardial I/R is unclear.
METHODS
In this study, we demonstrated that pretreatment with Tilianin dose-dependently
Tilianin Post-Conditioning Attenuates Myocardial Ischemia/Reperfusion Injury via Mitochondrial Protection and Inhibition of Apoptosis.
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BACKGROUND The aim of this study was to investigate the role of tilianin in modulating mitochondrial functions and mitochondria-mediated apoptosis during cardio-protection. MATERIAL AND METHODS Myocardial ischemia/reperfusion (I/R) injury was induced by 30 minutes coronary occlusion followed by two
Cardioprotective effects of tilianin in rat myocardial ischemia-reperfusion injury.
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Tilianin, the main effective flavonoid monomer enriched from Dracocephalum moldavuca L., has been shown to have cardioprotective effects. However, the mechanism of tilianin cardioprotection remains largely unknown. The present study aimed to investigate the effects of tilianin preconditioning on
Cardioprotection of tilianin ameliorates myocardial ischemia-reperfusion injury: Role of the apoptotic signaling pathway.
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Our previous research demonstrated that tilianin protects the myocardium in a myocardial ischemia reperfusion injury (MIRI) rat model and has prominent pharmacological potential as a cardiovascular drug. Our study aimed to investigate the molecular signaling implicated in the improvement of
Pretreatment with Tilianin improves mitochondrial energy metabolism and oxidative stress in rats with myocardial ischemia/reperfusion injury via AMPK/SIRT1/PGC-1 alpha signaling pathway.
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Mitochondrial energy metabolism and oxidative stress play a crucial role in ameliorating myocardial ischemia/reperfusion injury (MIRI). Tilianin has been reported to have a significant protection for mitochondrion in MIRI. However, the underlying mechanisms remain unknown. This study investigated
Tilianin-loaded Reactive Oxygen Species-Scavenging Nano-Micelles Protect H9c2 Cardiomyocyte Against Hypoxia/Reoxygenation-Induced Injury.
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Previous studies have shown that tilianin alleviates ischemia-reperfusion-induced cardiomyocyte injury. However, its clinical translation has been hampered because of its insolubility in water. Tilianin-based nano-micelles that may overcome this critical issue are presented. A polyethylene glycol
Improved oral delivery of tilianin through lipid-polymer hybrid nanoparticles to enhance bioavailability.
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Tilianin (TIL) may prevent and treat myocardial ischemia reperfusion injuries. However, its oral administration is hampered by its low bioavailability. The present study aimed to formulate lipid-polymer hybrid nanoparticles (LPHNs) as carriers for the sustained release and oral bioavailability
Tilianin mediates neuroprotection against ischemic injury by attenuating CaMKII-dependent mitochondrion-mediated apoptosis and MAPK/NF-κB signaling.
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OBJECTIVE
Tilianin, a naturally occurring flavonoid glycoside, possesses versatile biological activities including antioxidant, anti-inflammatory, energy collecting and anti-hypoxic effects. Little is known about the mechanisms underlying the effect of tilianin against ischemic injury in neuronal
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