A New Approach in the Treatment of Traumatic Brain Injury: The Effects of Levosimendan on Necrosis, Apoptosis, and Oxidative Stress
Küçük Resim Yok
Tarih
2022
Yazarlar
Dergi Başlığı
Dergi ISSN
Cilt Başlığı
Yayıncı
Elsevier Inc.
Erişim Hakkı
info:eu-repo/semantics/closedAccess
Özet
Objective: Traumatic brain injury (TBI) is an essential and common health problem worldwide. Levosimendan is an inotropic and vasodilator drug used to treat heart failure. Moreover, it exerts pleiotropic effects and, thus, protective effects on many organs. The present study aimed to investigate the effect of levosimendan on necrosis, apoptosis, and reactive oxygen species in rats with TBI. Methods: The study included 28 female Wistar-Albino rats weighing 200–250 g. The rats were divided into 4 groups with 7 rats each as follows: Group 1: No trauma group (Control), Group 2: Traumatized, untreated group (T), Group 3: Levosimendan was administered at a dose of 12 ?g/kg intraperitoneally 1 hour after the trauma (L1), Group 4: Levosimendan was administered at a dose of 12 ?g/kg intraperitoneally 2 hours after the concussion (L2). After the experiment, the rats were decapitated, and the brain tissue was removed. Necrosis was assessed with Cresyl violet staining, apoptosis was assessed with immunohistochemical analysis, superoxide dismutase and catalase levels were measured with the spectrophotometric method, and malondialdehyde (MDA) levels were assessed by High-Performance Liquid Chromatography. Results: The number of necrotic cells in the L1 and L2 groups was significantly lower than in the K and T groups (P = 0.015 and P = 0.03, respectively). Although the active caspase-3 level was signified considerably in the T, L1, and L2 groups compared to the K group, no significant difference was found among these 3 groups (P > 0.05). The results of superoxide dismutase levels were similar to those of active caspase-3. catalase level was significantly higher in the K group than in the T and L2 groups (P = 0.045). Malondialdehyde activity was considerably higher in the L1 and L2 groups compared to the K group (P = 0.023). Conclusions: Our results indicated that levosimendan may exert a neuroprotective effect by reducing necrosis in TBI and that levosimendan does not affect apoptosis and antioxidant levels in TBI. Comprehensive studies are needed to elucidate the effect of levosimendan on TBI fully. © 2022
Açıklama
Anahtar Kelimeler
Apoptosis, Levosimendan, Necrosis, Reactive oxygen species, Traumatic brain injury, adenosine triphosphate, caspase 3, catalase, levosimendan, malonaldehyde, reactive oxygen metabolite, superoxide dismutase, caspase 3, catalase, malonaldehyde, simendan, superoxide dismutase, animal cell, apoptosis, brain perfusion, brain tissue, cardiac muscle, cell count, concussion, Conference Paper, female, head injury, high performance liquid chromatography, hippocampus, histochemistry, image analysis, immunohistochemistry, immunoreactivity, necrosis, nonhuman, oxidative stress, oxygen consumption, prefrontal cortex, rat, spectrophotometry, staining, tissue homogenate, traumatic brain injury, Wistar rat, animal, apoptosis, metabolism, necrosis, Animals, Apoptosis, Brain Injuries, Traumatic, Caspase 3, Catalase, Female, Malondialdehyde, Necrosis, Oxidative Stress, Rats, Rats, Wistar, Simendan, Superoxide Dismutase
