apocynin


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apocynin

plant toxin found in Apocynum spp.; causes gastroenteritis.
References in periodicals archive ?
Apocynin improves oxygenation and increases eNOS in persistent pulmonary hypertension of the newborn.
Inhibiting NADPH oxidase by apocynin or atrovastatin treatment reduced the production of ROS and renal deposition of CaOx crystals in hyperoxaluric rats (Li et al.
Herein, we report the isolation of four new: vincetolate (1), vincetoside (2), vincetetrol (3), vincetomine (4) and seven know compounds: 1-(4-hydroxy-3-methoxyphenyl)-1,2,3,-propanetriol (5) [4,5], feruloyl-6-O-b-D-glucopyranoside (6) [6], apocynin (7) [7], 4-hydroxy-3,5-dimethoxybenzoic acid (8) [8], 7-megastigmene-3,5,6,9-tetrol (9) [9], qurcetin-3-O-b-D-glucopyranoside (10) [10], and 4-methoxy-kaempferol-3-O-b-D-glucopyranoside (11) [11] (Fig.
2], cells were pretreated with the nicotinamide adenine dinucleotide phosphate oxidase inhibitors apocynin or DPI, the epidermal growth factor receptor kinase activity inhibitor C56, the phosphoinositide 3-kinase activity inhibitors wortmannin or Ly294002, the Rac GTPase kinase inhibitor EHT 1864, or the mitochondrial uncoupler CCCP, prior to exposure to [Zn.
The NADPH oxidase inhibitor apocynin improves endothelial NO superoxide balance and lowers effectively blood pressure in spontaneously hypertensive rats: comparison to calcium channel blockade.
Purpose: To evaluate the effect of TGF-[beta] and the effect of apocynin on TGF-[beta]1 expression in skeletal muscle cells.
Co-administration of apocynin with lipoic acid enhances neuroprotection in a rat model of ischemia/reperfusion.
Simvastatin reverses target organ damage and oxidative stress in Angiotensin II hypertension: comparison with apocynin, tempol, and hydralazine.
Importantly, inhibition of NOX by apocynin significantly protected against PCB-mediated increase in epithelial permeability and alterations of ZO-1 protein expression.
In this study, we investigated the signaling cascade triggered by HOCl-alb that upregulates ICAM-1 expression in human umbilical vein endothelial cells (HUVECs) and whether an inhibitor of NOXs, apocynin, inhibits the biopathological effects of HOCl-alb.
Our results showed that inhibition of NADPH oxidase activity ameliorated cerebral ischaemia/reperfusion (I/R) injury and among Zn(2+) -dependent HDACs, HDAC4 and HDAC5 were significantly decreased both in vivo and in vitro, which can be reversed by NADPH oxidase inhibitor apocynin.