Role of Remifentanil on MAC, Bcl-2, and Bax Levels in Traumatic Brain Injury Rat Models

Abstract

Abstract: Introduction: Traumatic Brain Injury (TBI) conditions require immediate treatment such as the administration of analgesics and sedation, including remifentanil. TBI will affect the levels of several inflammatory and apoptotic proteins such as MAC, Bax, and Bcl-2. Remifentanil with its high affinity to μ-receptors is thought to affect the levels of these proteins and has neuroprotective properties to prevent secondary brain injury. Objectives: This research aims to determine the effect of giving remifentanil on MAC, Bcl-2, and Bax levels in rats with traumatic brain injury. Materials and Methods: Experimental research was conducted on 24 male Wistar rats, which were randomly divided into four groups. The Group-1 (G1) received an intravenous injection of NaCl, the Group-2 (G2) was given normal saline after TBI induction using the modified Feeney method. Furthermore, the Group-3 and Group-4 (G3 and G4) received fentanyl or remifentanil after TBI induction. The rat brain tissue was analyzed for MAC, Bcl-2, and Bax levels using the ELISA method. The data were analyzed statistically by ANOVA test, followed by Post-Hoc Multiple Comparison Test (p<0.05). Results: The MAC and Bax levels were reduced by the administration of fentanyl and remifentanil to TBI subjects, but increased Bcl-2 levels. The Post Hoc Multiple comparisons showed a significant difference between all group pairs (p<0.05). Meanwhile, the group given remifentanil showed more optimal results than those with fentanyl. Conclusion: The administration of remifentanil injection can act as a neuroprotector in TBI model Wistar rats by decreasing MAC and Bax levels and increasing Bcl-2 levels. Keywords: Bax, Bcl-2, MAC, Remifentanil, Traumatic brain injury.