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    Biochemical, pathological and ultrastructural investigation of whether lamotrigine has neuroprotective efficacy against spinal cord ischemia reperfusion injury
    (Elsevier Inc., 2021) Kahveci, Fatih Ozan; Kahveci, Ramazan; Gökçe, Emre Cemal; Gökçe, Aysun; Kısa, Üçler; Sargon, Mustafa Fevzi; Fesli, Ramazan; Sarı, Muhammed Fatih; Gürer, Bora
    Introduction: Lamotrigine, an anticonvulsant drug with inhibition properties of multi-ion channels, has been shown to be able to attenuates secondary neuronal damage by influencing different pathways. The aim of this study was to look into whether lamotrigine treatment could protect the spinal cord from experimental spinal cord ischemia-reperfusion injury. Materials and methods: Thirty-two rats, eight rats per group, were randomly assigned to the sham group in which only laparotomy was performed, and to the ischemia, methylprednisolone and lamotrigine groups, where the infrarenal aorta was clamped for thirty minutes to induce spinal cord ischemia-reperfusion injury. Tissue samples belonging to spinal cords were harvested from sacrificed animals twenty-four hours after reperfusion. Tumor necrosis factor-alpha levels, interleukin-1 beta levels, nitric oxide levels, superoxide dismutase activity, catalase activity, glutathione peroxidase activity, malondialdehyde levels and caspase-3 activity were studied. Light and electron microscopic evaluations were also performed to reveal the pathological alterations. Basso, Beattie, and Bresnahan locomotor scale and the inclined-plane test was used to evaluate neurofunctional status at the beginning of the study and just before the animals were sacrificed. Results: Lamotrigine treatment provided significant improvement in the neurofunctional status by preventing the increase in cytokine expression, increased lipid peroxidation and oxidative stress, depletion of antioxidant enzymes activity and increased apoptosis, all of which contributing to spinal cord damage through different paths after ischemia reperfusion injury. Furthermore, lamotrigine treatment has shown improved results concerning the histopathological and ultrastructural scores and the functional tests. Conclusion: These results proposed that lamotrigine may be a useful therapeutic agent to prevent the neuronal damage developing after spinal cord ischemia-reperfusion injury.
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    Neuroprotective effects of dexpanthenol on rabbit spinal cord ischemia/reperfusion injury model
    (Elsevier, 2022) Gülmez, Ahmet; Kuru Bektaşoğlu, Pınar; Tönge, Çağhan; Yaprak, Ahmet; Türkoğlu, Erhan; Önder, Evrim; İmge Ergüder, Berrin; Sargon, Mustafa; Gürer, Bora; Kertmen, Hayri
    Objective: Dexpanthenol (DXP) reportedly protects tissues against oxidative damage in various inflammation models. This study aimed to evaluate its effects on oxidative stress, inflammation, apoptosis, and neurological recovery in an experimental rabbit spinal cord ischemia/reperfusion injury (SCIRI) model. Methods: Rabbits were randomized into five groups of eight animals each: group 1 (control), group 2 (ischemia), group 3 (vehicle), group 4 (methylprednisolone, 30 mg/kg), and group 5 (DXP, 500 mg/kg). The control group underwent laparotomy only, whereas other groups were subjected to spinal cord ischemia by aortic occlusion (just caudal to the two renal arteries) for 20 min. After 24 h, a modified Tarlov scale was employed to record neurological examination results. Malondialdehyde and caspase-3 levels and catalase and myeloperoxidase activities were analyzed in tissue and serum samples. Xanthine oxidase activity was measured in the serum. Histopathological and ultrastructural evaluations were also performed on the spinal cord. Results: After SCIRI, serum and tissue malondialdehyde and caspase-3 levels and myeloperoxidase activity and serum xanthine oxidase activity were increased (p <0.05-0.001). However, serum and tissue catalase activity decreased significantly (p <0.001). DXP treatment was associated with lower malondialdehyde and caspase-3 levels and reduced myeloperoxidase and xanthine oxidase activities but increased catalase activity (p <0.05-0.001). Furthermore, DXP was associated with better histopathological, ultrastructural, and neurological outcome scores. Conclusion: This study was the first to evaluate antioxidant, anti-inflammatory, antiapoptotic, and neuroprotective effects of DXP on SCIRI. Further experimental and clinical investigations are warranted to confirm that DXP can be administered to treat SCIRI.
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    Possible anti-inflammatory, antioxidant, and neuroprotective effects of apigenin in the setting of mild traumatic brain injury: an investigation
    (Taylor and Francis Ltd., 2022) Kuru Bektaşoğlu, Pınar; Demir, Dilan; Koyuncuoğlu, Türkan; Yüksel, Meral; Peker Eyüboğlu, İrem; Karagöz Köroğlu, Ayça; Akakın, Dilek; Yıldırım, Alper; Çelikoğlu, Erhan; Gürer, Bora
    Objective: Apigenin is a plant flavone proven with biological properties such as anti-inflammatory, antioxidant, and antimicrobial effects. This study, it was aimed to examine the possible anti-inflammatory, antioxidant, and neuroprotective effects of apigenin in the setting of the mild traumatic brain injury (TBI) model. Methods: Wistar albino male rats were randomly assigned to groups: control (n = 9), TBI (n = 9), TBI + vehicle (n = 8), and TBI + apigenin (20 and 40 mg/kg, immediately after trauma; n = 6 and n = 7). TBI was performed by dropping a 300 g weight from a height of 1 m onto the skull under anesthesia. Neurological examination and tail suspension tests were applied before and 24 h after trauma, as well as Y-maze and object recognition tests, after that rats were decapitated. In brain tissue, luminol- and lucigenin-enhanced chemiluminescence levels and cytokine ELISA levels were measured. Histological damage was scored. Data were analyzed with one-way ANOVA. Results: After TBI, luminol (p <.001) and lucigenin (p <.001) levels increased, and luminol and lucigenin levels decreased with apigenin treatments (p <.01–.001). The tail suspension test score increased with trauma (p <.01). According to the pre-traumatic values, the number of entrances to the arms (p <.01) in the Y-maze decreased after trauma (p <.01). In the object recognition test, discrimination (p <.05) and recognition indexes (p <.05) decreased with trauma. There was no significant difference among trauma apigenin groups in behavioral tests. Interleukin (IL)-10 levels, one of the anti-inflammatory cytokines, decreased with trauma (p <.05), and increased with 20 and 40 mg apigenin treatment (p <.001 and p <.01, respectively). The histological damage score in the cortex was decreased in the apigenin 20 mg treatment group significantly (p <.05), but the decrease observed in the apigenin 40 mg group was not significant. Conclusion: The results of this study revealed that apigenin 20 and 40 mg treatment may have neuroprotective effects in mild TBI via decreasing the level of luminol and lucigenin and increasing the IL-10 levels. Additionally, apigenin 20 mg treatment ameliorated the trauma-induced cortical tissue damage.