Akademik Veri Yönetim Sistemi
Alkan T. (Yürütücü), Durak V. A., Cansev M., Çakır A., Aydin B.
Yükseköğretim Kurumları Destekli Proje, 2018 - 2020
Traumatic
brain injury (TBI) is a global emergency with high morbidity and mortality
rates. The pathophysiological processes of traumatic brain injury are
characterized by a sequential period of primary and secondary damage. While
primary brain damage happens immediately following trauma, secondary damage
develops hours or days later. Our study aims to investigate the neuroprotective
effects of uridine and/or hypothermia treatment, using oxidative, inflammatory,
and apoptotic parameters associated with the secondary damage period in a rat
model of traumatic brain injury.
Forty
male Sprague-Dawley rats were divided into five groups: Sham, TBI, TBI + uridine, TBI + hypothermia and
TBI + uridine + hypothermia. TBI was induced using the Marmarou
weight-drop method and mild hypothermia (32-34.0±1°C) was applied for 4 hours.
Uridine was administered intraperitoneally at 500mg/kg for 7 days following TBI.
Subsequently, brain tissue analyses were performed using TTC, Western Blot, and
ELISA kits.
We
found that catalase and MPO levels increased and GSH-px levels decreased in
rats with TBI. However, treatment with uridine and/or hypothermia resulted in
an increase in GSH-px levels and a decrease in catalase levels. The
hypothermia-administered groups exhibited an elevation in MPO level, but no
significant difference was observed with uridine treatment. No significant
differences were observed in the levels of SOD and MDA between the groups. Although
IL-1β and IL-6 levels were elevated in rats with traumatic brain injury, it was
found that these parameters decreased when uridine was administered alone or in
conjunction with hypothermia. Levels of IL-1β did not change by hypothermia
therapy alone. The TNF-α level was reduced significantly with combination
therapy. Poly ADP-ribose polymerase-1 (PARP-1), a protein involved in cell
death, was shown to be elevated following TBI and was reduced by hypothermia,
uridine, and the combined treatment, while levels of cleaved caspase-3 showed
no difference between groups.
The results of this study indicate that the combination of hypothermia and
uridine presents a promising therapeutic approach for TBI by reducing secondary
injury mechanisms. Nevertheless, ongoing research is required to concentrate on
the long-term effects of combined uridine and hypothermia therapy in clinical
settings and to optimize treatment protocols.