ELLAGIC ACID IMPROVED COGNITIVE DEFICIT, BRAIN ELECTROPHYSIOLOGY DECAY AND BRAIN CONTENT OF TNF-α IN RAT WITH TRAUMATIC BRAIN INJURY

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SARKAKI ALIREZA; Mashhadizadeh Shahram; FARBOOD YAGHOUB; DIANAT MAHIN; Khodadadi Alireza; KHAKSARI HADDAD MOHAMMAD

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Seminar: IRANIAN CONGRESS OF PHYSIOLOGY AND PHARMACOLOGY
Year:2015 | Issue:22

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Title

ELLAGIC ACID IMPROVED COGNITIVE DEFICIT, BRAIN ELECTROPHYSIOLOGY DECAY AND BRAIN CONTENT OF TNF-α IN RAT WITH TRAUMATIC BRAIN INJURY

Author(s)

Keywords

TRAUMATIC BRAIN INJURY

ELLAGIC ACID

COGNITION

BLOOD BRAIN BARRIER

TUMOR NECROSIS FACTOR-α

Abstract

INTRODUCTION: TRAUMATIC BRAIN INJURY (TBI) REMAINS A MAJOR CLINICAL PROBLEM GLOBALLY AND IS A MAJOR CAUSE OF DEATH AND DISABILITY IN MOST OF WORLD COUNTRIES. COGNITIVE DEFECTS SUCH AS LEARNING AND MEMORY IMPAIRMENT ARE AMONGST THE MOST FREQUENT SEQUELAE AFTER SEVERE AND MODERATE TBI. IT HAS BEEN SUGGESTED THAT ELLAGIC ACID (EA), A NATURAL PHENOL PRODUCT, EXHIBITS NEUROPROTECTIVE EFFECTS AGAINST INFLAMMATORY DAMAGE AFTER BRAIN INJURY. AIM OF THE PRESENT STUDY WAS EVALUATION OF THE EFFECT OF EA ON COGNITIVE AND BRAIN ELECTROPHYSIOLOGY DEFICITS INDUCED BY DIFFUSE TBI IN RATS.METHODS: THE ANIMAL MODEL OF TBI WAS INDUCED BY A 200 G WEIGHT WAS DROPPED THROUGH A FREE-FALLING TUBE ONTO THE HEAD OF ANESTHETIZED ANIMAL FROM A 2-M HEIGHT WHILE A STEEL DISC WAS ATTACHED TO THE ANIMALS’ SKULL. INTRAPERITONEAL INJECTION OF EA (100 MG/KG ONCE EVERY EIGHT HOURS DURING 48 H AFTER TRAUMA) WAS USED TO INVESTIGATE THE EFFECT OF EA ON MEMORY AND HIPPOCAMPAL LONG-TERM POTENTIATION (LTP). TO EXPLORE THE MECHANISMS UNDERLYING THE EFFECT OF EA ON BRAIN FUNCTION AFTER TBI, BRAIN CONTENT OF TNF-A AND BLOOD-BRAIN BARRIER (BBB) PERMEABILITY WERE DETERMINED.RESULTS: EA TREATMENT SIGNIFICANTLY (P<0. 001) REVERSED THE COGNITIVE AND ELECTROPHYSIOLOGY ABNORMALITIES OBSERVED AFTER TBI. FURTHERMORE EA DECREASED BRAIN CONTENT OF TNF-A AND BBB PERMEABILITY SIGNIFICANTLY (P<0.001) AFTER TBI WITH RESPECT TO SHAM GROUP.CONCLUSION: THESE FINDINGS SUGGEST THAT EA IMPROVED BRAIN INFLAMMATION FOLLOWING TBI AND IS ABLE TO RESTORE COGNITIVE, LTP DEFICITS THROUGH DECREASE BRAIN TNF-A LEVEL AND BBB PERMEABILITY.

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APA: Copy

SARKAKI, ALIREZA, Mashhadizadeh, Shahram, FARBOOD, YAGHOUB, DIANAT, MAHIN, Khodadadi, Alireza, & KHAKSARI HADDAD, MOHAMMAD. (2015). ELLAGIC ACID IMPROVED COGNITIVE DEFICIT, BRAIN ELECTROPHYSIOLOGY DECAY AND BRAIN CONTENT OF TNF-α IN RAT WITH TRAUMATIC BRAIN INJURY. IRANIAN CONGRESS OF PHYSIOLOGY AND PHARMACOLOGY. SID. https://sid.ir/paper/920692/en

Vancouver: Copy

SARKAKI ALIREZA, Mashhadizadeh Shahram, FARBOOD YAGHOUB, DIANAT MAHIN, Khodadadi Alireza, KHAKSARI HADDAD MOHAMMAD. ELLAGIC ACID IMPROVED COGNITIVE DEFICIT, BRAIN ELECTROPHYSIOLOGY DECAY AND BRAIN CONTENT OF TNF-α IN RAT WITH TRAUMATIC BRAIN INJURY. 2015. Available from: https://sid.ir/paper/920692/en

IEEE: Copy

ALIREZA SARKAKI, Shahram Mashhadizadeh, YAGHOUB FARBOOD, MAHIN DIANAT, Alireza Khodadadi, and MOHAMMAD KHAKSARI HADDAD, “ELLAGIC ACID IMPROVED COGNITIVE DEFICIT, BRAIN ELECTROPHYSIOLOGY DECAY AND BRAIN CONTENT OF TNF-α IN RAT WITH TRAUMATIC BRAIN INJURY,” presented at the IRANIAN CONGRESS OF PHYSIOLOGY AND PHARMACOLOGY. 2015, [Online]. Available: https://sid.ir/paper/920692/en

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