Related Experiment Video

Updated: Feb 11, 2026

Inducing Post-Traumatic Epilepsy in a Mouse Model of Repetitive Diffuse Traumatic Brain Injury
07:07

Inducing Post-Traumatic Epilepsy in a Mouse Model of Repetitive Diffuse Traumatic Brain Injury

Published on: February 10, 2020

11.3K

Ketamine ameliorates oxidative stress-induced apoptosis in experimental traumatic brain injury via the Nrf2 pathway

Jinwei Liang1, Shanhu Wu1, Wenxi Xie1

  • 1Department of Anesthesiology, The Second Affiliated Hospital of Fujian Medical University, Quanzhou, Fujian Province, People's Republic of China.

Drug Design, Development and Therapy
|May 2, 2018
PubMed
Abstract

Insights

Ketamine demonstrates neuroprotective effects against traumatic brain injury (TBI) by reducing oxidative stress and apoptosis. This study highlights ketamine

Area of Science:

  • Neuroscience
  • Pharmacology
  • Cellular Biology

Background:

  • Ketamine is a known neuroprotective agent, but its mechanism in treating traumatic brain injury (TBI) requires further elucidation.
  • Oxidative stress, cellular dysfunction, and apoptosis are key pathological features of TBI.

Purpose of the Study:

  • To investigate the neuroprotective effects of ketamine in TBI models.
  • To explore the role of the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway in ketamine's TBI treatment mechanism.

Main Methods:

  • A weight drop model was used to induce TBI in male wild-type mice.
  • Mice were divided into sham, TBI, and TBI + ketamine/vehicle groups, with ketamine administered via intraperitoneal injection.
  • Brain tissue was collected 24 hours post-injury for analysis.

Main Results:

  • Ketamine treatment significantly reduced neurological deficits, brain water content, and neuronal apoptosis in TBI mice.
  • Ketamine administration restored levels of oxidative stress markers (MDA, GPx, SOD) and increased Nrf2 protein expression.
  • The expression of Nrf2 downstream targets (hemeoxygenase-1, quinine oxidoreductase-1) was upregulated by ketamine.

Conclusions:

  • Ketamine effectively attenuates oxidative stress and apoptosis, thereby exerting neuroprotective effects post-TBI.
  • Ketamine shows potential as a therapeutic agent for treating traumatic brain injury.
Keywords:
Nrf2apoptosisketamineoxidative stresstraumatic brain injury

More Related Videos

Controlled Cortical Impact Model for Traumatic Brain Injury05:30

Controlled Cortical Impact Model for Traumatic Brain Injury

Published on: August 5, 2014

29.7K
A Novel Model of Mild Traumatic Brain Injury for Juvenile Rats07:36

A Novel Model of Mild Traumatic Brain Injury for Juvenile Rats

Published on: December 8, 2014

24.4K

Related Concept Videos

Post-traumatic Stress Disorder01:27

Post-traumatic Stress Disorder

Post-traumatic stress disorder (PTSD) is a psychiatric condition that arises following exposure to traumatic events such as natural disasters, forced displacement, or severe accidents. It significantly impairs individuals' ability to cope with daily activities and disrupts their emotional and psychological equilibrium.
Symptoms and Behavioral Manifestations
A spectrum of distressing symptoms characterizes PTSD. Recurrent flashbacks, where individuals involuntarily relive traumatic events,...
579
Nitric Oxide Signaling Pathway01:28

Nitric Oxide Signaling Pathway

Nitric oxide (NO), an inorganic gas, acts as a potent second messenger in most animal and plant tissues. NO diffuses out of the cells that produce it and enters the neighboring cells to generate a downstream response. NO synthase (NOS) catalyzes NO production by the deamination of the amino acid arginine. There are three isoforms of NOS. Endothelial cells have endothelial NOS (eNOS), nerve and muscle cells have neuronal NOS (nNOS), and macrophages produce inducible NOS (iNOS) upon exposure...
6.3K
Apoptosis01:30

Apoptosis

Apoptosis is a combination of two Greek words, 'apo' and 'ptosis,' meaning separation and falling off, respectively. Hippocrates used this word to describe gangrene, which was caused due to bandaging of fractured bones. Apoptosis was distinguished from necrosis in 1970 when John Kerr reported observations of morphological changes occurring during apoptosis. During one experiment, he observed that the disruption of blood supply to the liver tissue resulted in a size...
15.2K
Oxidation Numbers03:14

Oxidation Numbers

In redox reactions, the transfer of electrons occurs between reacting species. Electron transfer is described by a hypothetical number called the oxidation number (or oxidation state). It represents the effective charge of an atom or element, which is assigned using a set of rules.
43.0K
Pyruvate Oxidation01:15

Pyruvate Oxidation

After glycolysis, the charged pyruvate molecules enter the mitochondria via active transport and undergo three enzymatic reactions. These reactions ensure that pyruvate can enter the next metabolic pathway so that energy stored in the pyruvate molecules can be harnessed by the cells.
First, the enzyme pyruvate dehydrogenase removes the carboxyl group from pyruvate and releases it as carbon dioxide. The stripped molecule is then oxidized and releases electrons, which are then picked up by NAD+...
169.2K
C4 Pathway and CAM01:27

C4 Pathway and CAM

Most plants use the C3 pathway for carbon fixation. However, some plants, such as sugar cane, corn, and cacti that grow in hot conditions, use alternative pathways to fix carbon and conserve energy loss due to photorespiration. Photorespiration is the process that occurs when the oxygen concentration is high. Under such conditions, the rubisco enzyme in the Calvin cycle binds O2 instead of CO2, which halts photosynthesis and consumes energy.
C4 Pathway
The C4 pathway is used by plants such as...
49.3K