Gallic acid improved behavior, brain electrophysiology, and inflammation in a rat model of traumatic brain injury.

Abstract

Traumatic brain injury (TBI) is one of the main causes of intellectual and cognitive disabilities. In the clinic it is essential to limit the development of cognitive impairment after TBI. In this study, the effects of gallic acid (GA; 100 mg/kg, per oral, from 7 days before to 2 days after TBI induction) on neurological score, passive avoidance memory, long-term potentiation (LTP) deficits, and levels of proinflammatory cytokines including interleukin-1 beta (IL-1β), interleukin 6 (IL-6), and tumor necrosis factor-α (TNF-α) in the brain have been evaluated. Brain injury was induced following Marmarou's method. Data were analyzed by one-way and repeated measures ANOVA followed by Tukey's post-hoc test. The results indicated that memory was significantly impaired (p < 0.001) in the group treated with TBI + vehicle, together with deterioration of the hippocampal LTP and increased brain tissue levels of IL-1β, IL-6, and TNF-α. GA treatment significantly improved memory and LTP in the TBI rats. The brain tissue levels of IL-1β, IL-6, and TNF-α were significantly reduced (p < 0.001) in the group treated with GA. The results suggest that GA has neuroprotective properties against TBI-induced behavioral, electrophysiological, and inflammatory disorders, probably via the decrease of cerebral proinflammatory cytokines.

• Authors: Alireza Sarkaki, Yaghoub Farbood, Mohammad Kazem Gharib-Naseri, Mohammad Badavi, Mohammad Taghi Mansouri, Abbas Haghparast, Mohammad Ali Mirshekar
• Journal: Canadian journal of physiology and pharmacology (Can J Physiol Pharmacol) Vol. 93 Issue 8 Pg. 687-94 (Aug 2015) ISSN: 1205-7541 [Electronic] Canada
• PMID: 26222320 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Anti-Inflammatory Agents
• Cytokines
• Inflammation Mediators
• Neuroprotective Agents
• Gallic Acid

Topics

• Administration, Oral
• Animals
• Anti-Inflammatory Agents (administration & dosage, pharmacology)
• Behavior, Animal (drug effects)
• Brain (drug effects, metabolism, physiopathology)
• Brain Injuries (drug therapy, metabolism, physiopathology, psychology)
• Cytokines (metabolism)
• Disease Models, Animal
• Drug Administration Schedule
• Encephalitis (drug therapy, metabolism, physiopathology, psychology)
• Excitatory Postsynaptic Potentials (drug effects)
• Gallic Acid (administration & dosage, pharmacology)
• Inflammation Mediators (metabolism)
• Long-Term Potentiation (drug effects)
• Male
• Memory (drug effects)
• Neuroprotective Agents (administration & dosage, pharmacology)
• Rats, Wistar
• Recovery of Function
• Time Factors