How would Dexmedetomidine have Protective Effects on the Neurological Scores, Brain Edema and Brain-Blood Barrier Post to Serious Traumatic Brain Damage in Male Rats? (The Possible Role of MMP-9)
Journal Title: The 1st Annual Meeting of Georgian Center for Neuroscience Research - Year 2020, Vol 2, Issue 20
Abstract
Introduction: Dexmedetomidine DEX is known as a α2-adrenergic receptor agonist. It is used as a short-acting analgesic drug. In this study, we investigated the effects of neural protection of the DEX after induction of cerebral inflammation in rats. Materials and methods: The male Albino wistar rats received different doses of DEX (15, 30, 60 mg/kg, i.p.). All rats were intubated before TBI. In the TBI groups, diffuse TBI was induced by Marmarou method using a TBI induction device. The severe TBI was induced using a weight 300 gr. In the same groups, all stages of induction of TBI were performed except dropping weight on the head. The disruption of Blood brain- barrier (BBB) was evaluated 6 h post- TBI. The neurologic score (VCS) and brain water content, the beam-walk –balance task (WB) were determined before trauma, on trauma time(D0), and day 1 (D1) and Day 2 (D2) and Day 3 (D3) After TBI. after 72 hour CSF samples are collected from cisterna magna and then analysis mmp9 in CSF with Elisa assay. Results: Our results showed that traumatic brain injury led to significant brain edema and disrupt of blood brain- barrier and neurological defect and vestibular-motor dysfunction in the rat brain and increase mmp9 in CSF serum. DEX (15,30mg/kg) could attenuated brain edema, improved BBB, vestibular-motor dysfunction and decreased mmp9 in compare with TBI control group (P<0.001) but in 30mg/kg dose results were better and didn't have neuroprotective effect in 60mg/kg dose. Discussion: These findings showed that DEX has a prominent role in TBI outcome’s and perhaps protect neurons through modulating inflammatory and antioxidant pathways by inhibition of increasing intracellular calcium and decreasing mmp9 factor. By adding α2-adrenergic antagonist, neuroprotective effect of Dex has been disappeared. it indicates that a part of neuroprotective effect of DEX is through α2-adrenergic receptor.
Authors and Affiliations
Asal Safarbalou, Negar Mehrbakhsh, Mohaddese Shafiee Pour, Ali Siahposht Khachaki
Keywords
Related Articles
- EP ID EP677929
- DOI 10.29088/GCNR-2020.20
- Views 181
- Downloads 0
Effects of Quercetin Loaded Magnetic Nanoparticles on Electrophysiological and Behavioural Disturbances in the Animal Models of Epilepsy
Epilepsy is one of the most common neurological disorder, characterized by repetitive seizures and various mental health problems. Currently more than 30% of epilepsy cases are resistant to the treatment. It is believed...
Computational Lncrna – Mirna Interaction Analyses in Epilepsy Syndrome
Epilepsy is a neurological disorder associated to Central Nervous System. The seizures of epilepsy anomaly accurse due to the electrical activity disruption in the brain. Almost 80% of epilepsy cases are the results of...
The Comparison of Executive Functions in Addicts and Patients Under Buprenorphine Maintenance Treatment (BMT)
Introduction: Buprenorphine, a partial opioid agonist of the µ-receptor, is one of the most important developments in pharmacotherapy for opioid addiction. However, there are some clinical and empirical evidence for exe...
Nigella Sativa Oil Enhanced Motor Coordination in Phenol-Induced BALB/c Mice Models of Essential Tremor
Background: Essential tremor is a neuronal disorder characterized by uncontrollable tremor of different body parts. Nigella sativa is an established therapeutic plant in various ailments including neurological disorders...
The Neuroprotective Effect of Ursolic Acid Associated with Inflammation Factors: IL-10, IL β after the Induction of Severe Traumatic Brain Injury in Rats
Introduction: Ursolic Acid (UA) is a Penta cyclic triterpene compound which Reduces cerebral edema and improves neurological deficits after TBI, leading to increased Nrf2 protein and increased expression of reductase-1...