Open AccessThe Effects of Glucagon and Insulin Combination toward on Neurodegeneration Following Traumatic Brain Injury in Rat Model
Author(s) -
Akhmad Imron,
Bethy Hernowo,
Dany Hilmanto,
Kahdar Wiriadisastra,
Yulius Hermanto
Publication year - 2021
Publication title -
open access macedonian journal of medical sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.288
H-Index - 17
ISSN - 1857-9655
DOI - 10.3889/oamjms.2021.7490
Subject(s) - medicine , glucagon , traumatic brain injury , insulin , excitotoxicity , neuroprotection , endocrinology , glucose homeostasis , glutamate receptor , homeostasis , insulin resistance , receptor , psychiatry
BACKGROUND: Traumatic brain injury (TBI) is a major cause of death and disability in the productive age. Glutamate excitotoxicity and hyperglycemia those occur following TBI are among the factors those influence secondary brain injury.AIM: This study aimed to determine the effect of glucagon and insulin combination on neuronal necrosis following TBI.METHODS: A total of 28 male wistar rats were randomized into four experimental groups: placebo, insulin, glucagon, and combination of glucagon and insulin. Each animal underwent controlled cortical impact model of TBI. The blood glucose and glutamate levels were measured before and 4 h following TBI. The brain tissues were collected to evaluate neuronal necrosis.RESULTS: Glucagon or glucagon and insulin combination were able to prevent the increased of blood glutamate levels following TBI (p < 0.05). Glucagon administration was associated high blood glucose level (198.10 ± 32.58 mg/dL); a combination with insulin was able to minimize the increased of blood glucose level (166.53 ± 18.48 mg/dL). Combination of glucagon and insulin had a lower number of neuronal necrosis compare to the other groups (p < 0.005).CONCLUSION: The combination of glucagon and insulin potentially exhibit neuroprotection effect on rats following TBI as being demonstrated by lower number of neuronal necrosis. This finding further indicates the role of glucose homeostasis in neuroprotection.