tricin and Reperfusion-Injury

The objective of this study was to investigate the function and biological mechanisms of tricin in in-vivo damage to the myocardium produced by ischemia-reperfusion in LDLr -/- mice. The hypercholesterolemia animal model employed was male LDLr -/- mice. Coronary artery occlusion in mice resulted in the detection of oxidative stress and inflammatory pathology. In mice with coronary artery blockage, tricin reduced oxidative burden in the cardiac tissue and inflammatory mediators. Additionally, the ST segment of the animals receiving tricin was resumed. Tricine could dramatically lessen myocardial damage, according to pathological examination and triphenyltetrazolium chloride (TTC) staining. As a result of the research described above, the protective effects of tricin on myocardial injury have been explored, and the influence of inflammation and oxidative assaults in the ischemia-reperfusion injury (I/R) model of the heart has been demonstrated.

Topics: Animals; Heart; Male; Myocardium; Reperfusion; Reperfusion Injury

There have been several studies of nuclear factor-κB (NF-κB) and high-mobility group box1 (HMGB1) associated with the pathophysiology of cerebral ischemia. Tricin 7-glucoside, a major bioactive compound extracted from Sedum sarmentosum Bunge. The objectives of this study were to determine the effects of Tricin 7-glucoside on a cultured neuronal cell line, SH-SY5Y in vitro and experimental ischemic stroke in vivo. For oxygen-glucose deprivation (OGD) and tumor necrosis factor-α (TNF-α) stimulated SH-SY5Y cell line in vitro, SH-SY5Y cells were incubated with Tricin 7-glucoside. For in vivo experiment, rats were subjected to middle cerebral artery occlusion (MACO) for 1h, then followed by reperfusion for 23 h. Treatment of SH-SY5Y cells with Tricin 7-glucoside reduced the OGD-induced apoptosis and cytotoxicity, blocked TNF-α-induced NF-κB and IκB-α phosphorylation, and decreased HMGB1 expression. At doses higher than 50mg/kg, Tricin 7-glucoside produced a significant neuroprotective potential in rats with ischemia and reperfusion (I/R). Tricin 7-glucoside (100mg/kg) demonstrated significant neuroprotective activity even after delayed administration at 2h and 4h after I/R. Tricin 7-glucoside 100mg/kg attenuated histopathological damage, decreased brain edema, inhibited NF-κB activation and reduced HMGB1 expression. These data show that Tricin 7-glucoside protects brain against I/R injury with a favorable therapeutic time-window by alleviating cerebral I/R injury and attenuating blood-brain barrier (BBB) breakdown, and its protective effects may involve HMGB1 and NF-κB signaling pathway.

Topics: Animals; Apoptosis; Blood-Brain Barrier; Brain; Brain Ischemia; Cell Hypoxia; Cell Line; Cell Survival; Dose-Response Relationship, Drug; Down-Regulation; Flavonoids; Glucosides; HMGB1 Protein; Humans; Male; Neurons; Neuroprotective Agents; NF-kappa B; Random Allocation; Rats; Rats, Sprague-Dawley; Reperfusion Injury