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
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- EP ID EP677929
- DOI 10.29088/GCNR-2020.20
- Views 180
- Downloads 0
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