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Effects of 2″o-galloylhyperin on arrhythmias in an isolated tissue model of hypoxia and reperfusion
... unclear. 2 -O-GH, a main compound isolated from P. incarnata Fisch., has strong antioxidant activity and inhibited ischemia and reperfusion-induced arrhythmia (Feng et al., 2002;Wang et al., 2017). Inflammation is a complex processes triggered by foreign pathogens or tissue injury to eliminate harmful stimuli as well as to initiate the healing and repair process of the damaged tissue (Laveti et al., 2013). ...
2′-O-galloylhyperin, a major compound of Pyrola incarnata Fisch., possesses a variety of biological and pharmacological activities, including anti-oxidative and anti-inflammatory activities. Nevertheless, the underlying molecular mechanisms of 2′-O-GH in microbial infection and sepsis are not clear. In this study, we investigated the anti-inflammatory effects of 2′-O-GH. We found that 2′-O-GH significantly reduced the production of TNF-α, IL-6, and nitric oxide (NO), suppressed the expression levels of iNOS, blocked the translocation of NF-κB from the cytosol to nucleus, and decreased the MAPK activation in LPS-activated RAW 264.7 cells. 2′-O-GH also enhanced the nuclear translocation of Nrf2 and up-regulated the expression of heme oxygenase-1 (HO-1) and SIRT1. In addition, the administration of 2′-O-GH attenuated the TNF-α and IL-6 production in the serum, infiltration of inflammatory cells, liver tissue damage, and the mortality rate of LPS-challenged mice. Moreover, 2′-O-GH significantly upregulated Nrf2 and SIRT1 expression and inhibited the inflammatory responses in the liver of septic mice. The collective data indicate that 2′-O-GH could potentially be a novel functional food candidate in the treatment of sepsis.
2′-O-galloylhyperin (2′-O-GH), an active compound isolated from Pyrola calliantha, possesses remarkable antioxidant activity. The aims of this study were to investigate the hepatoprotective effect of 2′-O-GH against oxidative stress and elucidate the underlying mechanistic signaling pathways in HepG2 cells as well as in an animal model. Results showed that 2′-O-GH significantly inhibited hydrogen peroxide (H2O2)-induced HepG2 cell death in a dose dependent manner. The mitogen-activated protein kinase activation, ROS production, mitochondrial membrane potential, intracellular calcium level and subsequent apoptotic protein activation in H2O2-stimulated HepG2 cells were remarkably inhibited by 2′-O-GH. Furthermore, 2′-O-GH stimulation resulted in a fast and dramatic activation of Akt and nuclear translocation of the NF-E2-related factor 2 (Nrf2), along with the increased expression of heme oxygenase-1 (HO-1) and levels of glutathione (GSH). Meanwhile, histopathological evaluation of the liver also revealed that 2′-O-GH effectively ameliorated CCl4-induced the hepatic damage by reducing alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities. Therefore, these results suggested the hepatoprotective effect of 2′-O-GH might be correlated with its antioxidant and free radical scavenger effect.
An LC-MS/MS method was developed for the first time to simultaneously determine hyperoside and 2''-O-galloylhyperin, two major components in Pyrola calliantha extract, in rat plasma. Following extraction by one-step protein precipitation with methanol, the analytes were separated on a Venusil MP-C18 column within 2 min, using methanol-water-formic acid (50:50:0.1, v/v/v) as the mobile phase at a flow rate of 0.4 mL/min. Detection was performed on electrospray negative ionization mass spectrometry by multiple-reaction monitoring of the transitions of 2''-O-galloylhyperin at m/z 615.1 → 301.0, of hyperoside at m/z 463.1 → 300.1, and of internal standard at m/z 415.1 → 295.1. The limits of quantification were 2 ng/mL for both hyperoside and 2''-O-galloylhyperin. The precisions were <13.1%, and the accuracies were between -9.1 and 5.5% for both compounds. The method was successfully applied in pharmacokinetic studies following intravenous administration of the total flavonoids of P. calliantha extract in rats. Copyright © 2013 John Wiley & Sons, Ltd.
Electrical activity from endo- and epicardium was recorded from isolated segments of right ventricular free walls of guinea pigs using standard differential microelectrode techniques and a high-gain electrocardiogram (ECG). Stimulation was applied to the endocardium. Tissues were exposed to ischemic conditions for 10 min and then were reperfused with "normal" Tyrode's solution. Early premature beats or rapid ventricular tachycardia (VT) occurred in 36% of hearts during "ischemia" and 79% of hearts on reperfusion. Endocardial activation was not significantly slowed by ischemic conditions or reperfusion. However, transmural conduction times increased, and muscle action potential durations decreased during ischemic conditions and early reperfusion. Rapid VT began with alternating activation of endo- and epicardium, and continuous low-voltage ECG activity bridging diastole. Activation of epicardium was essential for occurrence of early premature beats and rapid VT. Hyperkalemia during ischemia promoted arrhythmias during "ischemia," but not during reperfusion. Oscillatory afterpotentials (OAP) also occurred during reperfusion (36%), but not during "ischemia". Our study provides an isolated tissue model that reproducibly generates tachycardias, and that permits study of ischemia and reperfusion-induced transmembrane activity and defects in transmural conduction.