Jove
Visualize
Contáctanos
JoVE
x logofacebook logolinkedin logoyoutube logo
ACERCA DE JoVE
Visión GeneralLiderazgoBlogCentro de Ayuda JoVE
AUTORES
Proceso de PublicaciónConsejo EditorialAlcance y PolíticasRevisión por ParesPreguntas FrecuentesEnviar
BIBLIOTECARIOS
TestimoniosSuscripcionesAccesoRecursosConsejo Asesor de BibliotecasPreguntas Frecuentes
INVESTIGACIÓN
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchivo
EDUCACIÓN
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualCentro de Recursos para ProfesoresSitio de Profesores
Términos y Condiciones de Uso
Política de Privacidad
Políticas

Videos de Conceptos Relacionados

Ligand-Gated Ion Channel Receptor: Gating Mechanism01:30

Ligand-Gated Ion Channel Receptor: Gating Mechanism

Ligand-gated ion channels are transmembrane proteins that play a vital role in intercellular communication and functions of the nervous system. They allow the influx of ions across the membrane once the neurotransmitter binds, allowing the subsequent transmission of electrical excitation across the neurons. Other ligand-gated ion channels, like the γ-aminobutyric acid (GABA) receptor, permit anions like chloride into the cells on the binding of the GABA molecule. Their entry into the cell...
Drugs Affecting Neurotransmitter Release or Uptake01:21

Drugs Affecting Neurotransmitter Release or Uptake

Certain drugs can affect how neurotransmitters called catecholamines, are released or taken back up in the adrenergic neuron. They can have different effects on the body's sympathetic transmission. Reserpine, a natural compound found in the Rauwolfia shrub, blocks a transporter called vesicular monoamine transporter (VMAT), which leads to a buildup of catecholamines in the cell and reduces sympathetic transmission. Another drug called guanethidine works in multiple ways, including blocking...
Drugs Affecting Neurotransmitter Synthesis01:29

Drugs Affecting Neurotransmitter Synthesis

Drugs affecting neurotransmitter synthesis can impact the adrenergic neuron and the synthesis of neurotransmitters. For example, α-methyltyrosine and carbidopa target specific enzymes involved in catecholamine synthesis. α-methyltyrosine inhibits the enzyme tyrosine hydroxylase, which converts tyrosine into dopamine. By blocking this enzyme, α-methyltyrosine reduces dopamine production and other catecholamines. Carbidopa, on the other hand, inhibits the enzyme dopa decarboxylase, which converts...
Cognitive Enhancers: Cholinesterase Inhibitors and NMDA Receptor Antagonists01:30

Cognitive Enhancers: Cholinesterase Inhibitors and NMDA Receptor Antagonists

Cognitive enhancers, also known as "smart drugs," are substances used to enhance memory, mental alertness, and concentration. These can be natural or synthetic and improve cognition in conditions like Alzheimer's disease (AD) and other neurodegenerative diseases. Some common examples include caffeine, amphetamines, methylphenidate, modafinil, arecoline, donepezil, vortioxetine, and piracetam. These enhancers work on the principle of synaptic plasticity and altered circuit function. They...
Alzheimer's Disease: Treatment01:22

Alzheimer's Disease: Treatment

Alzheimer's Disease (AD), a neurodegenerative disorder, is pathologically identified by amyloid plaques and neurofibrillary tangles composed of tau protein. AD pharmacotherapy aims to manage cognitive symptoms, delay disease progression, and treat behavioral symptoms. The treatment is primarily symptomatic and palliative, with no definitive disease-modifying therapy available. Cholinesterase inhibitors, including donepezil (Aricept), rivastigmine (Exelon), and galantamine (Razadyne), are...
Diabetic Neuropathy01:22

Diabetic Neuropathy

DefinitionDiabetic neuropathy is nerve damage caused by long-standing diabetes mellitus. It results directly from prolonged high blood sugar levels.PathophysiologyThe pathophysiology of diabetic neuropathy involves both metabolic and vascular disturbances triggered by chronic hyperglycemia.Metabolic injury: Elevated glucose levels activate the polyol pathway within nerve cells, leading to the accumulation of sorbitol and fructose. This increases oxidative stress, disrupts normal nerve...

También podría leer

Artículos Relacionados

Artículos vinculados a este trabajo por autores compartidos, revista y gráfico de citas.

Ordenar por
Same author

Recent Advances and Prospects of Succinate Dehydrogenase Inhibitor Acaricides.

Journal of agricultural and food chemistry·2026
Same author

Unwrapping the Dodecaborane Core: Structure, Electronic Properties, and Chemical Reactivity Across the Complete [B<sub>12</sub>I<sub><i>n</i></sub>]<sup>-</sup> Series (<i>n</i> = 11-1).

Journal of the American Chemical Society·2026
Same author

Tuning J-Aggregation Behavior of Fused Ring Acceptor Fluorophore within Nanoparticles for NIR-II Excitable Bioimaging with High Brightness.

ACS nano·2026
Same author

RNAi-Based Molecular Biopesticide: Inspired by Nature, Precision by Science, and Harmony to the Ecosystem.

Journal of agricultural and food chemistry·2026
Same author

Early Ferroptosis Detection Targeting Lipid Hydrogen Abstraction.

Journal of the American Chemical Society·2026
Same author

Unraveling the Electronic Structures of Platinum-Bromine Superhalogens: Photoelectron Spectroscopy of PtBr<sub><i>n</i></sub><sup>-</sup> (<i>n</i> = 2-5).

The journal of physical chemistry. A·2026

Video Experimental Relacionado

Updated: Jun 27, 2026

Oxygen-Glucose Deprivation and Reoxygenation as an In Vitro Ischemia-Reperfusion Injury Model for Studying Blood-Brain Barrier Dysfunction
08:56

Oxygen-Glucose Deprivation and Reoxygenation as an In Vitro Ischemia-Reperfusion Injury Model for Studying Blood-Brain Barrier Dysfunction

Published on: May 7, 2015

18.2K

Un donante de monóxido de carbono desencadenado por fluoro para mitigar el daño isquémico cerebral

Linfeng Xing1, Bin Wang2,3, Jin Li1

  • 1State Key Laboratory of Bioreactor Engineering, Shanghai Key Laboratory of Chemical Biology, School of Pharmacy, East China University of Science and Technology, Meilong Road 130, Shanghai 200237, China.

Journal of the American Chemical Society
|January 26, 2022
PubMed
Resumen

Este estudio introduce PCOD585, un nuevo compuesto que libera monóxido de carbono (CO) para proteger contra la lesión por isquemia-reperfusión. PCOD585 reduce efectivamente el daño cerebral y la muerte celular en modelos de accidente cerebrovascular.

Más Videos Relacionados

Experimental Models to Study the Neuroprotection of Acidic Postconditioning Against Cerebral Ischemia
10:13

Experimental Models to Study the Neuroprotection of Acidic Postconditioning Against Cerebral Ischemia

Published on: July 31, 2017

7.6K
Author Spotlight: Enhancing Cerebral Ischemia Research with a Simplified Rat Model
03:37

Author Spotlight: Enhancing Cerebral Ischemia Research with a Simplified Rat Model

Published on: July 5, 2024

746

Videos de Experimentos Relacionados

Last Updated: Jun 27, 2026

Oxygen-Glucose Deprivation and Reoxygenation as an In Vitro Ischemia-Reperfusion Injury Model for Studying Blood-Brain Barrier Dysfunction
08:56

Oxygen-Glucose Deprivation and Reoxygenation as an In Vitro Ischemia-Reperfusion Injury Model for Studying Blood-Brain Barrier Dysfunction

Published on: May 7, 2015

18.2K
Experimental Models to Study the Neuroprotection of Acidic Postconditioning Against Cerebral Ischemia
10:13

Experimental Models to Study the Neuroprotection of Acidic Postconditioning Against Cerebral Ischemia

Published on: July 31, 2017

7.6K
Author Spotlight: Enhancing Cerebral Ischemia Research with a Simplified Rat Model
03:37

Author Spotlight: Enhancing Cerebral Ischemia Research with a Simplified Rat Model

Published on: July 5, 2024

746

Área de la Ciencia:

  • Ingeniería biomédica
  • La neurociencia
  • Química

Sus antecedentes:

  • Las lesiones por isquemia-reperfusión (I/R) involucran especies reactivas dañinas de oxígeno como el peroxinitrito (ONOO-).
  • La eliminación directa de radicales altamente reactivos es un desafío; dirigirse a los ONOO- de mayor duración ofrece una estrategia preventiva.
  • El monóxido de carbono (CO) demuestra propiedades neuroprotectoras durante eventos isquémicos.

Objetivo del estudio:

  • Diseñar y sintetizar un nuevo donante de monóxido de carbono activado por ONOO, PCOD585, para posibles aplicaciones terapéuticas en lesiones de I/R.
  • Evaluar la capacidad de detección basada en la fluorescencia de PCOD585 para ONOO-.
  • Evaluar la eficacia neuroprotectora de PCOD585 en modelos celulares y animales de lesión cerebral.

Principales métodos:

  • Desarrollo de PCOD585 utilizando un andamio de xanteno enjaulado con carbono diseñado para la liberación de CO activada por ONOO.
  • Evaluación in vitro de los efectos citoprotectores de PCOD585 contra la privación de oxígeno y glucosa (OGD) en las células PC-12.
  • Evaluación in vivo de la permeabilidad de la barrera hematoencefálica y los efectos neuroprotectores de PCOD585 en un modelo de rata con oclusión de la arteria cerebral media (MCAO).

Principales resultados:

  • PCOD585 demostró una respuesta de activación por fluorescencia en la detección de ONOO, lo que permitió el monitoreo microscópico.
  • PCOD585 proporcionó una citoprotección significativa a las células PC-12 sometidas a OGD.
  • En ratas MCAO, PCOD585 redujo el volumen de infarto, disminuyó la apoptosis celular y mitigó el edema cerebral, lo que indica neuroprotección.

Conclusiones:

  • PCOD585 es un donante de CO activado por ONOO con doble funcionalidad como una sonda fluorescente.
  • El compuesto presenta prometedores efectos citoprotectores y neuroprotectores contra la lesión I/R, cruzando la barrera hematoencefálica.
  • PCOD585 representa una estrategia terapéutica potencial para mitigar el daño cerebral asociado con eventos isquémicos.