Background: It has been reported that curcumin, the main active compound of Curcuma longa, also known as turmeric, exhibits antinociceptive properties. The aim of this study was to examine the participation of ATP-sensitive potassium channels (K(ATP) channels) and, in particular, that of the L-arginine-nitric oxide-cyclic GMP-K(ATP) channel pathway, in the antinociceptive effect of curcumin.
Methods: Pain was induced by the intraplantar injection of 1% formalin in the right hind paw of Wistar rats. Formalin-induced flinching behavior was interpreted as an expression of nociception. The antinociceptive effect of oral curcumin was explored in the presence and absence of local pretreatment with L-NAME, an inhibitor of nitric oxide synthase, ODQ, an inhibitor of soluble guanylyl cyclase, and glibenclamide, a blocker of K(ATP) channels.
Results: Oral curcumin produced a dose-dependent antinociceptive effect in the 1% formalin test. Curcumin-induced antinociception was not altered by local L-NAME or ODQ, but was significantly impaired by glibenclamide.
Conclusions: Our results confirm that curcumin is an effective antinociceptive agent. Curcumin-induced antinociception appears to involve the participation of K(ATP) channels at the peripheral level, as local injection of glibenclamide prevented its effect. Activation of K(ATP) channels, however, does not occur by activation of the L-arginine-nitric oxide-cGMP-K(ATP) channel pathway.
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http://dx.doi.org/10.3344/kjp.2012.25.4.221 | DOI Listing |
Cell Calcium
December 2024
Department of Physiology and Cell Biology, University of Nevada Reno School of Medicine, Reno, NV, 89557, USA. Electronic address:
Interstitial cells of Cajal in the plane of the myenteric plexus (ICC-MY) serve as electrical pacemakers in the stomach and small intestine. A similar population of cells is found in the colon, but these cells do not appear to generate regular slow wave potentials, as characteristic in more proximal gut regions. Ca handling mechanisms in ICC-MY of the mouse proximal colon were studied using confocal imaging of muscles from animals expressing GCaMP6f exclusively in ICC.
View Article and Find Full Text PDFFront Endocrinol (Lausanne)
January 2025
Department of Clinical and Biomedical Science, University of Exeter Medical School, Exeter, United Kingdom.
Introduction: Congenital Hyperinsulinism (CHI) has not been previously studied in Ukraine. We therefore aimed to elucidate the genetics, clinical phenotype, histological subtype, treatment and long-term outcomes of Ukrainian patients with CHI.
Methods: Forty-one patients with CHI were recruited to the Ukrainian national registry between the years 2014-2023.
Am J Physiol Heart Circ Physiol
December 2024
Wells Center for Pediatric Research, Department of Pediatrics, Indiana University School of Medicine, Indianapolis, IN, USA.
Missense mutations in calmodulin (CaM)-encoding genes are associated with life-threatening ventricular arrhythmia syndromes. Here, we investigated a role of cardiac K channel dysregulation in arrhythmogenic long QT syndrome (LQTS) using a knock-in mouse model heterozygous for a recurrent mutation (p.N98S) in the gene (Calm1).
View Article and Find Full Text PDFMed J Armed Forces India
December 2024
Director & Commandant, Armed Forces Medical College, Pune, India.
Neonatal diabetes mellitus is a rare disorder with prevalence of one in 400,000 live births that's defined by persistent hyperglycaemia within the first six months of life. Neonatal diabetes is heterogeneous and can be transient or permanent. Developmental delay, Epilepsy and Neonatal Diabetes (DEND) syndrome is characterised by developmental delay, epilepsy, and neonatal diabetes.
View Article and Find Full Text PDFNeuropharmacology
December 2024
Department of Pharmacology, Medical School of Southeast University, Nanjing, China. Electronic address:
Epilepsy, a prevalent neurological disorder characterized by spontaneous recurrent seizures, significantly impacts physiological and cognitive functions. Emerging evidence suggests a crucial role for metabolic factors, particularly lactate, in epilepsy. We discuss the applicability of the astrocyte-neuron lactate shuttle (ANLS) model during acute seizure events and examine lactate's metabolic adaptation in epilepsy progression.
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