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Страница 1 од 61 резултати
Treatment with NADPH oxidase inhibitor apocynin alleviates diabetic neuropathic pain in rats.
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Increased reactive oxygen species by the activation of NADPH oxidase (NOX) contributes to the development of diabetic complications. Apocynin, a NOX inhibitor, increases sciatic nerve conductance and blood flow in diabetic rats. We investigated potential protective effect of apocynin in rat diabetic
Oral treatment with the NADPH oxidase antagonist apocynin mitigates clinical and pathological features of parkinsonism in the MPTP marmoset model.
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This study evaluates the therapeutic efficacy of the NADPH oxidase inhibitor apocynin, isolated as principal bioactive component from the medicinal plant Picrorhiza kurroa, in a marmoset MPTP model of Parkinson's disease (PD). The methoxy-substituted catechol apocynin has a similar structure as
Apocynin protects retina cells from ultraviolet radiation damage via inducing sirtuin 1.
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Direct exposure to Ultraviolet (UV) radiation causes progressive damages in retinal cells, which is one of the hypothetical mechanisms underlying age-related retinopathy or macular degeneration. The protective effects of Apocynin against UV damages were firstly tested in retinal pigment epithelium
Microglial NADPH oxidase activation mediates rod cell death in the retinal degeneration in rd mice.
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Accumulating evidence supports that nicotinamide adenine dinucleotide phosphate (NADPH) oxidase contributes to microglia-mediated neurotoxicity in the CNS neurodegenerative diseases. Several studies, including ours, suggest that microglial activation is involved in the retinal degeneration in the
Adrenergic and serotonin receptors affect retinal superoxide generation in diabetic mice: relationship to capillary degeneration and permeability.
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Reactive oxygen species play an important role in the pathogenesis of diabetic retinopathy. We studied the role of adrenergic and serotonin receptors in the generation of superoxide by retina and 661W retinal cells in high glucose and of the α1-adrenergic receptor (AR) on vascular lesions of the
Anti-inflammatory and neuroprotective effects of an orally active apocynin derivative in pre-clinical models of Parkinson's disease.
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BACKGROUND
Parkinson's disease (PD) is a devastating neurodegenerative disorder characterized by progressive motor debilitation, which affects several million people worldwide. Recent evidence suggests that glial cell activation and its inflammatory response may contribute to the progressive
AQP4 KO exacerbating renal dysfunction is mediated by endoplasmic reticulum stress and p66Shc and is attenuated by apocynin and endothelin antagonist CPU0213.
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Aquaporin 4 (AQP4) is essential in normal kidney. We hypothesized that AQP4 knockout (KO) may exacerbate pro-inflammatory factors in the stress induced renal insufficiency. Mechanisms underlying are likely due to activating renal oxidative stress adaptor p66Shc and endoplasmic reticulum (ER) stress
NADPH Oxidase Contributes to Photoreceptor Degeneration in Constitutively Active RAC1 Mice.
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The active form of small GTPase RAC1 is required for activation of NADPH oxidase (NOX), which in turn generates reactive oxygen species (ROS) in nonphagocytic cells. We explored whether NOX-induced oxidative stress contributes to rod degeneration in retinas expressing constitutively active (CA)
Protective effect of apocynin on antimycin A-induced cell damage in osteoblastic MC3T3-E1 cells.
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Apocynin is a naturally occurring methoxy-substituted catechol, experimentally used as an inhibitor of NADPH-oxidase. In the present study, we investigated the protective effects of apocynin on antimycin A (AMA)-induced toxicicy in osteoblastic MC3T3-E1 cells. Exposure of MC3T3-E1 cells to AMA
NADPH oxidase hyperactivity induces plantaris atrophy in heart failure rats.
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BACKGROUND
Skeletal muscle wasting is associated with poor prognosis and increased mortality in heart failure (HF) patients. Glycolytic muscles are more susceptible to catabolic wasting than oxidative ones. This is particularly important in HF since glycolytic muscle wasting is associated with
Apocynin attenuates cholesterol oxidation product-induced programmed cell death by suppressing NF-κB-mediated cell death process in differentiated PC12 cells.
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Cholesterol oxidation products are suggested to be involved in neuronal degeneration. Apocynin has demonstrated to have anti-inflammatory and anti-oxidant effects. We assessed the effect of apocynin on the cholesterol oxidation product-induced programmed cell death in neuronal cells using
The neuroprotective effects of apocynin.
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The recognition of health benefits of phytomedicines and herbal supplements lead to an increased interest to understand the cellular and molecular basis of their biological activities. Apocynin (4-hydroxy-3-methoxy-acetophenone) is a constituent of the Himalayan medicinal herb Picrorhiza kurroa
Advanced oxidation protein products accelerate bone deterioration in aged rats.
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Advanced oxidation protein products (AOPPs) are novel markers of oxidation-mediated protein damage, and accumulation of AOPPs is involved in many pathophysiological conditions. Our previous studies demonstrated that the serum level of AOPPs negatively correlated with the age-related change in bone
Apocynin attenuates diaphragm oxidative stress and protease activation during prolonged mechanical ventilation.
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OBJECTIVE
To investigate whether apocynin protects the diaphragm from wasting and oxidative stress during mechanical ventilation (MV).
METHODS
Prospective, randomized, controlled study.
METHODS
Research laboratory.
METHODS
Adult female Sprague-Dawley rats.
METHODS
Rats were randomly assigned to one
Apocynin protects against global cerebral ischemia-reperfusion-induced oxidative stress and injury in the gerbil hippocampus.
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Increased production of reactive oxygen species (ROS) following cerebral ischemia-reperfusion (I/R) is an important underlying cause for neuronal injury leading to delayed neuronal death (DND). In this study, apocynin, a specific inhibitor for NADPH oxidase, was used to test whether suppression of
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