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Capsaicin regulates vascular endothelial cell growth factor expression by modulation of hypoxia inducing factor-1alpha in human malignant melanoma cells.
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OBJECTIVE
Capsaicin (8-Methyl-N-Vanillyl-6-nonenamide), a known natural dietary chemopreventive agent, inhibits malignant melanoma cell proliferation. In the present study, we examined the effect of capsaicin on constitutive and induced vascular endothelial cell growth factor (VEGF) expression in
Sensory CGRP depletion by capsaicin exacerbates hypoxia-induced pulmonary hypertension in rats.
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Pulmonary hypertension is a debilitating disease that occurs among infants and adults. One of many etiologies is airway hypoxia. We previously demonstrated a role of endogenous calcitonin gene-related peptide (CGRP), a potent vasodilator, in ameliorating the pulmonary vascular pressor response to
Differential effects of acute hypoxia on the activation of TRPV1 by capsaicin and acidic pH.
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Transient receptor potential vanilloid 1 (TRPV1) is a Ca(2+)-permeable cation channel activated by a variety of physicochemical stimuli. The effect of hypoxia (P(O(2)), 3%) on rat TRPV1 overexpressed in HEK293T has been studied. The basal TRPV1 current (I (TRPV1)) was partly activated by hypoxia,
Acute hypoxia prolongs the apnea induced by right atrial injection of capsaicin.
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Inspiratory central drive is augmented by acute hypoxia that leads to a hyperventilation, but it is inhibited by capsaicin (Cap)-induced stimulation of pulmonary C fibers (PCFs) that produces an expiratory apnea. We hypothesized that acute hypoxia should shorten or eliminate the Cap-induced apnea.
Minute ventilation during hypoxia is augmented with capsaicin supplementation in aged mice.
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Capsaicin is an agonist for transient receptor potential vanilloid 1 (TRPV1), and acute injection results in an increased frequency and tidal volume in young rats. It is unknown how capsaicin influences breathing in aged mice. We tested the hypothesis that capsaicin supplementation would elicit an
Ventilatory responses to hypoxia and hypercapnia in awake rats pretreated with capsaicin.
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Ventilatory responses to hypoxia and hypercapnia were measured by indirect plethysmography in unanesthetized unrestrained adult rats injected neonatally with capsaicin (50 mg/kg) or vehicle. Such capsaicin treatment ablates a subpopulation of primary afferent fibers containing substance P and
Capsaicin Protects Cardiomyocytes against Anoxia/Reoxygenation Injury via Preventing Mitochondrial Dysfunction Mediated by SIRT1.
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Capsaicin (Cap) has been reported to have beneficial effects on cardiovascular system, but the mechanisms underlying these effects are still poorly understood. Apoptosis has been shown to be involved in mitochondrial dysfunction, and upregulating expression of SIRT1 can inhibit the apoptosis of
Protection of capsaicin against hypoxia-reoxygenation-induced apoptosis of rat hippocampal neurons.
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The aim of this study was to investigate the effect of capsaicin on hypoxia-reoxygenation (H/R)-induced apoptosis in primary rat hippocampal neurons. Three hours of hypoxia (1% O2) and subsequent reoxygenation for 24 h significantly increased the apoptotic death of hippocampal neurons, as evidenced
Capsaicin prevents mitochondrial damage, protects cardiomyocytes subjected to anoxia/reoxygenation injury mediated by 14-3-3η/Bcl-2.
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Capsaicin(Cap) is an active component of chili peppers that is extracted from capsicum plants. Recent studies have reported that Cap can ameliorate myocardial ischemia/reperfusion(I/R) injury. Mitochondria play an important role in pathways of apoptosis induced by myocardial I/R injury. However, the
Role of substance P in rat carotid body responses to hypoxia and capsaicin.
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Role of sensory C fibers in hypoxia/reoxygenation-impaired myogenic constriction of cerebral arteries.
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OBJECTIVE
Hypoxia/reoxygenation (H/R) associated with extracorporeal membrane oxygenation disrupts cerebral autoregulation. However, the underlying mechanisms remain poorly understood. The present study was designed to investigate the role of sensory C-fibers in myogenic responsiveness of cerebral
Modulation of autoregulatory escape by capsaicin-sensitive afferent nerves in rat stomach.
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Visceral C fibers are stimulated by ischemia and hypoxia, which can be produced by intense vasoconstriction. Epinephrine applied to the gastric submucosa produces a marked vasoconstriction followed by autoregulatory escape. We hypothesize that the autoregulatory escape from epinephrine-induced
Attenuation of isocapnic hyperpnoea-induced guinea-pig bronchoconstriction by chronic hypoxia.
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Chronic hypoxia has been shown to augment the production of antioxidants in rat lungs and to reduce airway hyperreactivity in patients with asthma. This study investigated indirectly whether this increase in antioxidants occurs in guinea-pig lungs and whether the increased antioxidants affect
Esophagoprotective activity of angiotensin-(1-7) in experimental model of acute reflux esophagitis. Evidence for the role of nitric oxide, sensory nerves, hypoxia-inducible factor-1alpha and proinflammatory cytokines.
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Gastroesophageal reflux disease (GERD) is a global disease rapidly increasing among world population. The pathogenesis of reflux esophagitis which is considered as the early stage of GERD is complex, resulting from an imbalance between aggressive factors damaging the esophagus and a number of the
[Morphological parameters of the liver in rats during changes in nitric oxide content and deafferentation with capsaicin].
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The aim of this investigation was to study the morphological changes of rat liver during the blockade of nitric oxide (NO) synthesis and its increased content in the intact rats and after the damage of capsaicin-sensitive nerves. It was shown that the damage of capsaicin-sensitive nerves resulted in
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